AntiDiabetic Cancer Research Results
AntiDiabetic, AntiDiabetic: Click to Expand ⟱
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AntiDiabetic
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Scientific Papers found: Click to Expand⟱
*cardioP↑, Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation - PMC
*MitoP↑, The mechanism included promotion of mitophagy, which reduced generation of mitochondrial ROS and accumulation of damaged mitochondria[31].
*ROS↓, AS-IV can reduce ROS-mediated autophagosome accumulation and myocardial injury caused by I/R[21]
*mtDam↓,
*neuroP↓, Ischemic stroke MCAO in SD rats; OGD/R in HT22 cells A neuroprotective role (-) apoptosis (+) autophagy
TumAuto↓, For NSCLC cells treated with cisplatin, AS-IV inhibited the increased autophagy of proteins Beclin1 and LC3 I/II
*AntiDiabetic↑, Protective effect of AS-IV on diabetes
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Liver, |
HepG2 |
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AntiCan↑, The PGE-AgNPs showed a dose-dependent response against human liver cancer cells (HepG2) (IC50; 70 μg/mL) indicating its greater efficacy in killing cancer cells.
Dose↝, surface charge of synthesized AgNPs was highly negative (−26.6 mV) and particle size distribution was ranging from ∼35 to 60 nm and the average particle size was about 48 nm determined by dynamic light scattering (DLS)
*antiOx↑, literature suggests that AgNPs display considerable antioxidant activity in vitro
*AntiDiabetic↑, Antidiabetic potential of biosynthesized AgNPs
*Bacteria↓, Synergistic antibacterial potential of AgNPs with standard antibiotics
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ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier
*Inflam↓, It has anti-inflammatory, rheumatological, ulcer inhibiting, anticholinergic, analgesic, antimicrobial, antistress, antidiabetes, anticancer, liver protection, anthelmintics, antioxidants, antifungal, and wound healing propertie
*AntiBio↑,
*AntiDiabetic↑,
*hepatoP↑,
*antiOx↑,
*AntiFungal↑,
*Wound Healing↑,
*other↑, Garlic has a higher concentration of sulfur compounds (allicin, diallyl disulfide, S-allylcysteine, and diallyl trisulfide), which are responsible for its therapeutic properties.
*BP↓, Garlic consumption lowers blood pressure, inhibits atherosclerosis, decreases serum cholesterol and triglycerides, suppresses platelet aggregation, and increases fibrinolytic activity, among other things
*LDL↓,
*AntiAg↑,
*cognitive↑, Garlic can also aid in preventing cognitive decline by shielding neurons from neurotoxicity and apoptosis, which helps to prevent ischemia, obsessive-compulsive disorder (OCD), and neuronal death while also boosting learning and memory retention
*memory↑,
Risk↑, People who consumed more garlic had a 54% decreased risk of pancreatic cancer than those who consumed fewer amounts of garlic
*COX1↓, Garlic supplements have been demonstrated to reduce cyclooxygenase activity and thromboxane A2 production, resulting in antiplatelet action
*TXA2↓,
*LDL↓, Indeed, clinical studies on healthy subjects have evidenced that standardized garlic treatment (900 mg/day) significantly reduces total cholesterol (TC) and low-density lipoprotein cholesterol (c-LDL).
*antiOx↑, Multiple studies have focused on allicin therapeutic potential as an antioxidant (inducing antioxidant product production),
AntiCan↑, anticancer (triggering cancer cells apoptosis and inhibiting tumor growth),
*cardioP↑, cardioprotective (decreasing angiogenesis and inducing vasorelaxation)
*BP↓, Conversely, aged garlic extract supplementation was shown to be more effective than the placebo in lowering systolic blood pressure
*Weight↓, Garlic powder supplementation (800 mg/daily) resulted in a significant decrease in body weight and body fat mass (
NK cell↑, Actually, aged garlic administration in patients with advanced cancer of the digestive system led to an improvement of natural killer (NK) cell activity but did not cause improvement in QoL
*AntiDiabetic↑, Actually, daily garlic allicin supplementation (0.05–1.5 g) displayed a positive and sustained role in blood glucose, total cholesterol (TC), and high/low density lipoprotein (HDL-c/LDL-c) regulation in type 2 diabetes mellitus (T2DM) management
*GSH↑, 2-month application of coated garlic powder tablets (900 mg with alliin and allicin contents of 1.3% and 0.6%, respectively), the glutathione (GSH) concentration significantly increased in circulating human erythrocytes
*antiOx↑, Astaxanthin (ASTA) is a kind of food-derived active ingredient (FDAI) with antioxidant and antidiabetic functions.
*AntiDiabetic↑,
*toxicity∅, It is nontoxic but its poor solubility and low bioavailability hinder its application in the food industry.
*BioAv↓,
*BioAv↑, n this study, a novel carrier, polyethylene glycol-grafted chitosan (PEG-g-CS) was applied to enhance the bioavailability of astaxanthin.
Apoptosis↑, Astaxanthin causes apoptosis in
several in vitro studies, including both oral and liver cancer cells
EMT↓, AXT inhibits the EMT pathway in colon cancer cells and can reduce breast cancer cells' proliferation and growth
AntiCan↑, Astaxanthin can address human health problems, including cancer, cardiovascular, and neurodegenerative diseases.
*cardioP↑,
*neuroP↑,
TumCG↓, 100 mg/kg Astaxanthin strongly inhibited tumor growth relative to the TC group, with an inhibitory rate of 41.7%.
*antiOx↑, .ASX is often referred to as the "super antioxidant" since it has the strongest antioxidant activity of current carotenoids.
*Bacteria↓, Studies have demonstrated antioxidant and antimicrobial, immunomodulatory, hepatoprotective, anticancer, and antidiabetic effects of ASX.
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
ROS↓, Astaxanthin and carbendazim function in conjunction to inhibit cell proliferation while reducing ROS production in
breast cancer cells.
*chemoPv↑, Chemopreventive and therapeutic efficacy of astaxanthin against cancer
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*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].
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*BioAv↓, Biochanin A (BCA) is an isoflavone mainly found in red clover with poor solubility and oral absorption
*Inflam↓, various effects, including anti-inflammatory, estrogen-like, and glucose and lipid metabolism modulatory activity, as well as cancer preventive, neuroprotective, and drug interaction effects.
AntiCan↑,
*neuroP↑, many studies have focused on the effect of BCA on neurodegenerative diseases, especially PD and AD
chemoPv↑, BCA Has Chemopreventive Activity Against Various Cancers
Dose↝, BCA is metabolized in the gut to GEN or formononetin, which is converted to daidzein and then to equol (Knight and Eden, 1996).
*SOD↑, BCA also has a gastroprotective effect through the enhancement of cellular metabolic cycles, as evidenced by increases in superoxide dismutase (SOD) and nitric oxide (NO) activity, decreases in the malondialdehyde (MDA) and Bax levels, and increases
*MDA↓,
*BAX↓,
*HSP70/HSPA5↑, and increases in Hsp70 expression
*AntiDiabetic↑, BCA is well known for its antidiabetic and hypolipidemic effects.
*Insulin↑, BCA increases the circulating insulin levels and improves insulin sensitivity, leading to body weight control, an increase in liver glycogen, and a decrease in plasma glucose
*TNF-α↓, BCA inhibits the production of inflammatory mediators, such as TNF-α, interleukin-1β (IL-1β), IL-6, iNOS, COX-2, MMP-9, and NO, in various inflammatory responses
*IL1β↓,
*IL6↓,
*iNOS↓,
*COX2↓,
*MMP9↓,
*ROS↓, BCA scavenges ROS and increases SOD activity
*PGE2↓, BCA significantly reduces the synthesis of prostaglandin E2 and/or thromboxane B2 by inhibiting COX-2 expression
*BACE↓, BCA effectively inhibits the activity of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1)
*BioAv↑, Various attempts have been made to improve the solubility and bioavailability of BCA, including the use of liposomes
P-gp⇅, Interestingly, BCA has been found to stimulate P-gp in some studies (An and Morris, 2010). Therefore, the effect of BCA on P-gp may be substrate dependent.
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*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.
*memory↑, Bacopa monnieri has been used for centuries in Ayurvedic medicine, alone or in combination with other herbs, as a memory and learning enhancer, sedative, and anti-epileptic.
*neuroP↑, Brahmi as a lead formulation for treating neurological disorders and exerting cognitive-enhancing effects.
*cognitive↑,
*hepatoP↑, figure 1
*antiOx↑,
*AntiDiabetic↑,
*fatigue↓,
*GSK‐3β↓, figure 3
*PI3K↑,
*Akt↑,
*tau↓,
*ROS↓, The neuroprotective properties of these bioactive components include reduction of ROS, neuroinflammation, aggregation inhibition of amyloid-β and improvement of cognitive and learning behavior.
*Inflam↓,
*glucose↓, OGTT showed that plasma glucose levels in volunteers who received capsicum were significantly lower than those in the placebo group at 30 and 45 minutes
*Insulin↑, Furthermore, plasma insulin levels were significantly higher at 60, 75, 105, and 120 minutes
*Dose↑, 5 grams of capsicum presented capsaicin levels that were associated with a decrease in plasma glucose levels and the maintenance of insulin levels.
*AntiDiabetic↑, The present result might have clinical implications in the management of type 2 diabetes
*Bacteria↓, properties including anti-viral, anti-bacterial, anti-cancer, immunomodulatory, and wound-healing activities.
*AntiCan↑,
*Imm↑,
*Wound Healing↑,
*NF-kB↓, including inhibition of the transcription factors NF-κB
*5LO↓, use of CAPE in diabetes therapy have shown that caffeic acid phenethyl ester inhibits the enzyme 5-lipoxygenase
*AntiDiabetic↑, Antidiabetic Properties
ChemoSen↑, CAPE treatment enhances the antitumor effect of cytostatic drugs, such as vinblastine, paclitacol, estramustine and docetaxel, used in the chemotherapy of prostate cancer [76,81,82].
selectivity↑, CAPE acts selectively on diseased cells, without adversely affecting normal cells [88]
chemoPv↑, CAPE may be useful as support for cancer therapy in terms of chemoprevention of non-cancerous cells
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TRPM7↓, investigated the effects of the TRPM7 inhibitor carvacrol on the viability, resistance to apoptosis, migration, and invasiveness of the human U87 glioblastoma cell line
tumCV↓, Carvacrol treatment reduced the viability, migration and invasion of U87 cells.
TumCMig↓, Carvacrol reduces U87 cell migration and invasion
TumCI↓, Carvacrol inhibited U87 cell migration, invasion and MMP-2 protein expression.
MMP2↓, Carvacrol also decreased MMP-2 protein expression and promoted the phosphorylation of cofilin.
toxicity↓, It's oral LD50 is 810 mg/kg in rats [26] and it is a “generally recognized as safe” food flavor additive according to the United States Food and Drug Administration.
*Inflam↓, carvacrol exhibits anti-inflammatory, antidiabetic, antinociceptive, cardioprotective, neuroprotective and anticarcinogenic properties [27]
AntiDiabetic↑,
cardioP↑,
neuroP↑,
selectivity↑, Carvacrol (CAR) blocked TRPM7 currents in HEK293 cells overexpressing TRPM7 and TRPM7-like currents in U87 cells.
Apoptosis↑, Carvacrol induces apoptosis in U87 cells
p‑Cofilin↑, Carvacrol upregulates phosphorylation of cofilin (p-cofilin) and reduces polymerization of F-actin
F-actin↓,
PI3K↓, Carvacrol suppresses PI3K/Akt and MEK/MAPK signaling pathways
Akt↓,
MEK↓,
MAPK↓,
*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions
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*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,
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Ovarian, |
SKOV3 |
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Ovarian, |
OVCAR-3 |
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TumCMig↓, At sub-toxic concentrations (<0.5 µM), celastrol inhibited migration and invasion in a concentration-dependent manner in SKOV-3 and OVCAR-3 cells.
TumCI↓,
NF-kB↓, celastrol blocked the canonical NF-κB pathway by inhibiting IκBα phosphorylation, and preventing IκBα degradation and p65 accumulation.
p65↓, blocking p65 translocation
MMP9↓, protein MMP-9, but not MMP-2, were inhibited by celastrol.
eff↑, Furthermore, celastrol showed no synergistic effect with MG132, an NF-κB inhibitor.
AntiTum↑, showing antitumor, anti-inflammatory, antihypertensive and antidiabetic activities
Inflam↓,
AntiDiabetic↑,
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AntiCan↑, C. asiatica possesses a broad array of therapeutic effects including anti-ulcer, anti-cancer, anti-diabetic, anti-osteoporotic, neuroprotective, antioxidant, cardioprotective, and anti-inflammatory activities.
*AntiDiabetic↑,
*neuroP↑,
*antiOx↑,
*cardioP↑,
*Inflam↓,
*hepatoP↑, figure 1
*AntiAge↑,
*AST↓,
*ALAT↓,
*LDH↓,
*lipid-P↓,
Casp3↑, anti-cancer fig 1
*memory↑, 1000 mg/kg/d of Centella extract in drinking water improved the deficit's executive function, learning, and recognition memory in aged mice and also attenuated the increased anxiety observed in female mice.
*Wound Healing↑, C. asiatica may accelerate the healing process of wounds by promoting angiogenesis.
eff↑, Fard et al. made silver nanoparticles from C.asiatica leaf extract to study how these nanoparticles kill cancer cells and cause them to commit suicide in the MCF-7 breast cancer cell line.
*neuroP↑, According to the literature survey, C. asiatica (gotu kola) has been reported to have a comprehensive neuroprotection by different modes of action such as enzyme inhibition, prevention of amyloid plaque formation in Alzheimer's disease, dopamine neur
*Aβ↓,
*ROS↓, dopamine neurotoxicity in Parkinson's disease, and decreasing oxidative stress.
*Wound Healing↑, Monographs of the plant describing mainly its wound healing and memory enhancement effects exist in the European Pharmacopeia
*memory↑,
*Inflam↓, anti-inflammatory [8, 9], antipsoriatic [10], antiulcer [11, 12], hepatoprotective
*hepatoP↑,
*Imm↑, anticonvulsant [14], sedative [15], immunostimulant [16], cardioprotective [17, 18], antidiabetic [19], cytotoxic and antitumor [20, 21], antiviral [22], antibacterial [23], insecticidal [24], antifungal [25], antioxidant
*cardioP↑,
*AntiDiabetic↑,
*AntiFungal↑,
*antiOx↑,
*Dose↝, Presence of several flavonoid derivatives such as quercetin, kaempferol, patuletin, rutin, apigenin, castilliferol (Figure 3), castillicetin, and myricetin has been reported in C. asiatica [35, 39, 42], while isolation of polysaccharides (e.g., cente
*AChE↓, The extract was found to inhibit AChE with 50% of inhibition rate at 150 μg/mL concentration . only the standardized extract was found to inhibit AChE
*BChE↓, ethanol extracts of the plant samples from Turkey and India exerted 46.95 ± 0.94% and 70.30 ± 3.77% against BChE, respectively, and a notable inhibition against TYRO
*Tyro3↓,
*lipid-P↓, showing a neuroprotective effect in old rats by way of bringing about a significant decrease in PCO contents and lipid peroxidation.
*BioAv↝, madecassoside, asiaticoside, madecassic acid, and asiatic acid are widely distributed in the body and madecassoside, asiaticoside may exert their biological activity through converted into aglycone (madecassic acid, and asiatic acid).
*BioAv↝, C. asiatica enhances the function of the nervous system. It dissolves in methanol, ethanol, and water.
*MDA↓, Male Wistar rats – MDA ↓, GSH ↑, SOD ↑, AChE↓
*GSH↑,
*SOD↑,
*AChE↓,
*memory↑, Male SD rats; hippocampal cell – Spatial working memory↑, Ki-67 cells↑
*Ki-67↑,
*Catalase↑, Male SD rats MAPK SOD↑, LPO↑, CAT↑, GSH↑, dopamine↑, glutamate↑, Syn1↑, Stx1A↑, PI3K↑, PDK1↑, PEBP↓, VMAT2↑, TH ↑, MAPK ↑, BDNF↑, NGF↑
*PI3K↑,
*BDNF↑,
*NGF↑,
*ROS↓, Water extract of CA Tg2576 mice – ROS↓, NRF2↑, GCLC↑, HMOX1↑, NQO1↑, ATP↑, Mt-ND1↑, Mt-ATP6↑, Mt-CO1↑, Mt-CYB↑, oxygen consumption rate↑
*NRF2↑,
*HO-1↑,
*NQO1↑,
*ATP↑,
*OCR↑,
*TNF-α↓, Ethanolic extract of CA Male SD rats – TNF-α↓, BDNF↑
*PP2A↑, Ethanolic extract of CA Male albino Wistar rats PP2A/GSK-3B PP2A↑, GSK-3B↓, Bcl-2↑
*GSK‐3β↓,
*Bcl-2↑,
*TrkB↑, Standardized extract of CA Male Wistar rats – NR2A↑, NR2B↑, BDNF↑,TrkB↑
*NOTCH1↑, Asiatic acid Male SD rats – Notch1↑, SOX2↑, DCX↑, Nrf2↑, nestin↑, p21 positive cells↓, MDA↓
*SOX2↑,
*Nestin↑,
*MDA↓,
*MAOA↓, Asiaticoside-D Worms – MAO-A↓, MAO-B↓
*MAOB↓,
*GPx↑, Previous studies found that C. asiatica and its triterpenoids could effectively increase SOD and GPX activities, activate nuclear factor erythroid-2-related factor 2, improve the cognitive impairment of animals,
*cognitive↑,
*ROS↓, C. asiatica and its triterpenoids could reduce ROS production
*neuroP↑, they reduced related nerve cell apoptosis, increased synaptic density, and improved the survival rate of neural cells
*glucose↓, Methanol extract of CA Male SD rats – Blood glucose ↓, food and water intake ↓, ALT↓, AST↓, PFK ↑, GS ↑, GP↑, glycogen content ↑
*ALAT↓,
*AST↓,
*PFK↓,
*Weight↓, inhibit weight gain
*Inflam↓, (4) ameliorate inflammation,
*AntiDiabetic↑, C. asiatica extract and related components (asiatic acid, madecassoside) for the treatment of endocrine diseases such as diabetes, obesity and osteoporosis are excellent.
*Obesity↓,
*Wound Healing↑, The C. asiatica extract and its triterpenoids had certain therapeutic and relieving effects on acne, baldness, vitiligo, atopic dermatitis, and wounds. C. asiatica extract can effectively promote wound healing in diabetic patients
*cardioP↑, C. asiatica has a positive effect on cardiovascular diseases.
*GutMicro↑, C. asiatica and its triterpenoids also have therapeutic effects on digestive disorders, which is mainly reflected by improved liver fibrosis, colitis, and gastric mucosal damage; and even reduced Helicobacter pylori gastric colonization
*Sepsis↓, Asiatic acid can improve the side effects caused by antibiotics, reverse multidrug resistance (MDR), and reduce sepsis.
*BioAv↑, C. asiatica cream containing 5.12% asiaticoside and 5.1% madecassoside can be completely absorbed by the skin and effectively improve pigmentation and may be used in treating hypertrophic scars
*antiOx↑, including anti-oxidant, anti-inflammatory, antilipidemic, antidiabetic, and antihypertensive activities.
*Inflam↓,
*AntiDiabetic↑,
*Obesity↓, chlorogenic acid as a nutraceutical for the prevention and treatment of metabolic syndrome and associated disorders, including in vivo studies, clinical trials, and mechanisms of action
*Wound Healing↑, It was found that chlorogenic acid accelerated wound healing.
*BP↓, Significant reductions of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were observed
*Dose↝, A total of 23 healthy subjects (four men and 19 women) were given water (control) and 400 mg of chlorogenic acid dissolved in 200 mL of low nitrate water.
*ROS↓, the mechanism proposed was that chlorogenic acid scavenges reactive oxygen species (ROS) generated by consumption of high-fat diet, which suppresses the expression of inflammation, and consequently reduces fat accumulation,
*Fas↓, chlorogenic acid supplementation in high-fat diet-induced-obese mice significantly inhibited fatty acid synthase (FAS),
*HMG-CoA↓, As for hypercholesterolemia, chlorogenic acid has been found to inhibit 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR)
*GutMicro↑, high-CGAs coffee (80.8 mg) induced a significant increase in the growth of Bifidobacterium spp. as well as Clostridium coccoides-Eubacterium rectale group, the latter group having also potential to benefit human health.
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antiOx↑, CGAs have been associated with health benefits, such as antioxidant, antiviral, antibacterial, anticancer, and anti-inflammatory activity, and others that reduce the risk of cardiovascular diseases, type 2 diabetes, and Alzheimer’s disease.
*Bacteria↓,
AntiCan↑,
*Inflam↓,
*cardioP↑, reduce the risk of cardiovascular disease by suppressing the expression of P-selectin in platelets
*AntiDiabetic↑,
*GutMicro↑, non-absorbed part of 5-CQA and caffeic acid in the human gastrointestinal tract serves as a substrate for beneficial intestinal microbiota,
*eff↑, The fortification of foods with coffee CGAs has the potential to improve the functionality of foods.
*eff↑, exposing them to monopolar pulses of 2 Hz with an interval of 0.5 s and generating an electric field of 28 kV/10 cm with water at 20 °C. The use of an electric field increased radical scavenging activity up to 31% and 11%, for green and roasted coffe
*ROS↓, CGAs are known to exhibit a radical scavenging effect similar to ascorbic acid
*IronCh↑, CGAs can chelate transition metals such as Fe2+ to scavenge free radicals and disrupt chain reactions
*neuroP↑, The neuroprotective mechanisms of coffee are suggested to be related to the anti-inflammatory effects of caffeine and CGAs on A1 and A2 receptors.
*AChE↓, some coffee compounds could inhibit brain acetylcholinesterase and butyrylcholinesterase
*BChE↓,
*chemoPv↑, Several mechanisms have suggested that CGAs may have a chemopreventive effect
*BioAv⇅, the absorption and bioavailability of CGAs are controversial due to the significant interindividual differences regarding their utilization, metabolism, and excretion found in scientific and clinical studies
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*neuroP↑, including neuroprotection for neurodegenerative disorders and diabetic peripheral neuropathy, anti-inflammation, anti-oxidation, anti-pathogens, mitigation of cardiovascular disorders,
*Inflam↓,
*antiOx↑,
*cardioP↑, Cardiovascular Protective Effect
*NRF2↑, pivotal antioxidants by activating the Nrf2 pathway
*AMPK↑, It elevates AMPK pathways for the maintenance and restoration of metabolic homeostasis of glucose and lipids.
*SOD↑, figure1
*Catalase↑,
*GSH↑,
*GPx↑,
*ROS↓,
*TNF-α↓,
*IL6↓,
*NF-kB↓,
*COX2↓,
*glucose↓, CGA can attenuate glucose absorption
*TRPC1↓, CGA suppresses the levels of transient receptor potential canonical channel 1 (TRPC1) and decreases ROS and Ca2+, thus mitigating lysophosphatidylcholine (LPC)-induced endothelial injuries
*Ca+2↓,
*HO-1↑, enhancing superoxide dismutase (SOD), and producing NO and heme oxygenase (HO)-1
*NF-kB↓, CGAs can regulate NF-κB and PPARα pathways, lower HIF-1α expression, and suppress cardiac apoptotic signaling, thus executing beneficial effects against cardiac hypertrophy
*PPARα↝,
*Hif1a↓,
*JNK↓, CGA can inhibit NF-κB and JNK pathways, exhibiting cardioprotection
*BP↓, GCE (93 or 185 mg for 4 weeks) could lead to a reduction of 4.7 and 5.6 mmHg in levels of systolic blood pressure (SBP) and a decrease of 3.3 and 3.9 mmHg in levels of diastolic blood pressure (DBP)
*AntiDiabetic↑, CGA has shown its functions in protecting β cells from apoptosis, improving β cell function, facilitating glycemic control, and mitigating DM complications.
*hepatoP↑, CGA can mediate hepatoprotective roles in various pathological conditions of the liver via antioxidant and anti-inflammatory features
*TLR4↓, (1) It can inhibit TLR4-mediated activation of NF-κB, thus suppressing pro-inflammatory responses;
*NRF2↑, (3) it can increase the activity of the Nrf2 pathway
*Casp↓, (4) it can inhibit caspases’ activation to suppress hepatic apoptosis induced by chemicals or toxins.
*neuroP↑, CGA has shown diverse neuroprotective effects on various neuropathological conditions which may be exerted through inhibition of neuroinflammation, reduction in ROS production, prevention of oxidation, and suppression of neuronal apoptosis
*Aβ↓, CGA or extracts containing CGA can inhibit Aβ aggregation-caused cellular injury in SH-SY5Y cells, a neuroblastoma cell line
*LDH↓, CGA increases survival and decreases apoptosis via decreasing activities of lactate dehydrogenase (LDH) and the levels of MDA and raising the levels of SOD and GSH-Px
*MDA↓,
*memory↑, CGA prevents Aβ deposition and neuronal loss and ameliorates learning and memory deterioration in APP/PS2 mice
*AChE↓, CGA inhibits acetylcholinesterase (AChE) activity in rat brains, suggesting its beneficial effect against cognitive impairment
*eff↑, CGA protects against injury caused by cerebral ischemia/reperfusion
EMT↝, It also modulates the epithelial–mesenchymal transition (EMT) process of breast cancer cells by downregulation of N-cadherin and upregulation of E-cadherin
N-cadherin↓,
E-cadherin↑,
TumCCA↑, CGA can stall the cells in the S phase and cause DNA injury in human colon cancer cell lines such as HCT116 and HT29 by increasing ROS production, upregulation of phosphorylated p53, HO-1, and Nrf2
ROS↑,
p‑P53↑,
HO-1↑,
NRF2↑,
ChemoSen↑, CGA in combination with doxorubicin suppresses cellular metabolic activity, colony formation, and cell growth of U2OS and MG-63 cells by upregulating caspase-3 and PARP and suppressing the p44/42 MAPK pathway, thus inducing apoptosis
mtDam↑, mechanism involves CGA-mediated excessive ROS production, causing mitochondrial dysfunction, leading to increases in cleaved levels of caspase-3, caspase-9, PARP, and Bax/Bcl-2 ratio
Casp3↑,
Casp9↑,
PARP↑,
Bax:Bcl2↑,
TumCG↓, in vivo experiments showing that CGA can reduce tumor growth and volume in pancreatic cancer cell-bearing nude mice by modifying cancer cell metabolism through decreasing levels of cyclin D1, c-Myc, and cyclin-dependent kinase-2 (CDK-2),
cycD1/CCND1↓,
cMyc↓,
CDK2↓,
mitResp↓, interrupting mitochondrial respiration, and suppressing aerobic glycolysis
Glycolysis↓,
Hif1a↓, CGA arrests cells at the phase of G1 and inhibits cell viability of prostate cancer cell DU145 by suppressing the levels of HIF-1α and SPHK-1, PCNA, cyclin-D, CDK-4, p-Akt, p-GSK-3β, and VEGF
PCNA↓,
p‑GSK‐3β↓,
VEGF↓,
PI3K↓, inhibition of the PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,
OS↑, Extending Lifespan in Worms
*AntiDiabetic↑, Epidemiological and intervention studies suggest that they can reduce the risk of developing type 2 diabetes and cardiovascular disease
*BioAv↑, absorption of intact acyl-quinic acids in the small intestine
is feasible
*toxicity↓, which indicated no significant evidence of toxic or adverse effects following acute oral exposure
*antiOx↑, CQAs have antioxidant [68], antibacterial [69], antiviral [70], antidiabetic [71], neuroprotective [72,73], anti-inflammatory [74], and cytostatic effects [75,76].
*Bacteria↓,
*AntiDiabetic↑,
*neuroP↑, Several in vivo studies have demonstrated the neuroprotective properties of 5-CQA
*Inflam↓,
*cardioP↑, CQAs have been used therapeutically in some clinical treatments as well, e.g., in the treatment of cardiovascular diseases [77] and arterial hypertension (high blood pressure)
*BP↓,
*other↓, CQA (i.g.) in doses of 50–200 mg/kg bw (aluminum chloride (AlCl3), 35 mg/kg bw per day) weakens aluminum-induced Al3+-accumulation, oxidative stress, mitochondrial damage, and nuclear pyknosis in the hippocampus
eff↓, Chlorogenic acid has been found to counteract the effects of metformin, a pharmaceutical drug used to manage elevated blood sugar levels. only observed at high levels of chlorogenic acid, which is unlikely to occur in humans
*BioAv↓, CGA’s oral bioavailability remains limited, prompting research into optimized extraction methods, novel formulations, and structural modifications.
*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, hepatoprotective, cardioprotective and neuroprotective effects, and modulation of lipid and glucose metabolism
*Inflam↓,
*Bacteria↓,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*ROS↓, CGA action include inhibition of oxidative stress, regulation of inflammatory responses through modulation of the NF-κB pathway and activation of the Nrf2 pathway
*NF-kB↓, inhibition of NF-κB
*NRF2↑,
*Obesity↓, Research demonstrates that CGA may influence body weight regulation through multiple pathways, including modulation of gut microbiota, reduction of inflammation, regulation of adipogenesis, and stimulation of thermogenesis.
*GutMicro↑, increasing the abundance of probiotic bacteria such as Bifidobacterium and Lactobacillus, while reducing the abundance of bacterial strains found in obese patients and animals, such as Desulfovibrionaceae, Ruminococcaceae, Lachnospiraceae, and Erysip
*AntiAg↑, antiplatelet effects of CGA are supported by both in vitro and in vivo studies
*cardioP↑, CGA was recognized as a compound with high cardioprotective potential, considering its antioxidant, anti-inflammatory, and antihypertensive activities
*AntiDiabetic↑, CGA alleviates the effects of type 2 diabetes mellitus (DM) and helps prevent its development
*NLRP3↓, CGA also inhibits the NLRP3 inflammasome via Nrf2 activation, significantly decreasing proteinuria, creatinine, and urea levels in diabetic rats
*OCLN↓, figure 3
*VEGF↓,
BioAv↝, CGA is water-soluble but highly unstable when exposed to elevated temperature, light, oxygen, or alkaline pH
AntiCan↑, chlorogenic acid (CHA) possesses several pharmacological attributes, such as anticancer, hepatoprotective, antimicrobial, immune-suppressant, antioxidant, and antidiabetic activities.
*hepatoP↑,
*Bacteria↓,
*antiOx↓,
*AntiDiabetic↑,
Apoptosis↓, It can hinder the process of cell division, trigger cell apoptosis, and suppress an increase in cancerous cell growth.
TumCG↓,
angioG↓, mechanisms include angiogenesis, invasion and migration, oxidative stress, inflammation, cell cycle arrest, and proliferation.
TumCI↓,
TumCMig↓,
ROS↝,
Inflam↝,
*antiOx↑, Antioxidant effects of cocoa may directly influence insulin resistance and, in turn, reduce risk for diabetes.
*AntiDiabetic↑,
*cognitive↑, beneficial effects on satiety, cognitive function, and mood.
*AntiAg↑, Bordeaux and colleagues found that, among healthy participants in a platelet function study, those who had consumed chocolate before testing (n=141) had reduced platelet activity compared to nonconsumers.
*AntiAg↑, dark chocolate consumption decreased platelet adhesion 2 h after consumption in 22 heart transplant patients
*LDL↓, ll three significantly improved LDL and HDL levels from baseline in subjects with high LDL at the start of the study.
*HDL↑, in another trial, HDL increased by 11.4% and 13.7% when subjects consumed dark chocolate and polyphenol-enriched dark chocolate
*BP↓, A relationship between cocoa consumption and reduced BP was first observed in the Zutphen Elderly Study. A 2010 study found that a daily dose of 1052 mg cocoa flavanols was required to reduce 24-h ambulatory BP
*eff↓, Rimbach et al. noted that beneficial effects on BP, FMD, and platelet aggregation have not been found in all human trials (67, 73). Further, improvements are often small when they are observed
*ROS↓, Cocoa intake increases serum antioxidant capacity, protecting the endothelium from oxidative stress and endogenous ROS
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Inflam↓, various cancers has been demonstrated and it modulates cell signaling pathways, including inflammation, angiogenesis, apoptosis, autophagy, and the cell cycle.
angioG↓,
Apoptosis↑,
TumAuto↑,
TumCCA↑,
BioAv↓, Despite its promising pharmacological activities, the clinical utility of chrysin remains limited due to its poor bioavailability, low solubility, limited permeability, and rapid metabolism.
Half-Life↓,
BioAv↓, The oral bioavailability of chrysin has been reported to range from 0.003% to 0.02%, with a maximum plasma concentration between 12 and 64 nM
*ROS↓, The study reported that chrysin administration protected the kidneys and liver of rats from oxidative damage induced by chronic ethanol consumption
*hepatoP↑, Hepatoprotective Potential
*RenoP↑, The renal protective effect of chrysin was related to increasing the antioxidant enzyme activities and decreasing the regulation of serum renal toxicity markers.
TET1↑, chrysin meaningfully induced the expression of TET1 in GC cells.
MMP9↓, hrysin might contribute to its anticancer effects by regulating MMP-9 expression.
cMyc↓, Both c-Myc and Ki-67 expressions were found to be suppressed in the tumor tissues treated with chrysin and G1-treated tumor tissues
Ki-67↓,
CBR1↓, chrysin directly interacts with CBR1, inhibiting its enzymatic activity at both the molecular and cellular levels.
ROS↑, This inhibition led to elevated intracellular ROS levels, triggering ROS-dependent autophagy
ChemoSen↑, chrysin enhances pancreatic cancer cell sensitivity to gemcitabine by inducing ferroptosis death, both in vitro and in vivo
Bax:Bcl2↑, chrysin increased the Bax/Bcl-2 expression ratio in ATC cells following treatment
PUMA↑, PUMA and Notch-1 were activated, and Slug was inactivated by chrysin treatment
NOTCH1↑,
*AntiDiabetic↑, Anti-Diabetic Potential
*neuroP↑, Neuroprotective Effects
*GABA↑, treatment of chrysin improves levels of GABA, monoamines, glutamic acid, and their metabolites in three brain regions, while also inhibiting DNA fragmentation markers like 8-HdG as well as BDNF.
*DNAdam↓,
*BDNF↑,
*memory↑, protective effects of chrysin against memory impairments associated with hippocampal neurogenesis
*AGEs↓, figure 6
*Aβ↓,
*cardioP↑, Cardioprotective Effects
*AntiArt↑, Anti-Arthritis Potential
eff↑, combination potential was higher than apigenin or chrysin alone.
eff↑, combination of quercetin enhanced the toxic effects of chrysin on the cell lines
*eff↑, neuroprotective synergistic effects of chrysin and kaempferol revealed therapeutic potential in mitigating cerebral ischemi
RadioS↑, study reported that treatment of MDA-MB-231 cells with chrysin in combination with radiation therapy (RT) caused synergistic antitumor properties.
eff↑, the combination of metformin and chrysin demonstrated pronounced synergistic cytotoxic effects on cancer cells
ChemoSen↑, chrysin was combined with a low dose of cisplatin, the resulting growth inhibition was significantly enhanced.
eff↑, demonstrating greater potency than chrysin or silver nanoparticles alone [198].
*AntiBio↑, Its broad-spectrum antimicrobial activity, targeting both Gram-positive and Gram-negative bacteria as well as various fungi, positions TCA as a potent natural antimicrobial agent.
*AntiFungal↓,
*AntiDiabetic↑, TCA demonstrates promising antidiabetic and anti-inflammatory activities
*Inflam↓,
*ROS↑, Antimicrobial: TCA has been shown to induce reactive oxygen species (ROS) overload and oxidative stress
ROS↑, Anticancer Activity:TCA is associated with the increase in ROS and FE as a result of a reversible accumulation of cells in the G2/M cell cycle phases
TumCCA↑,
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*neuroP↑, This versatile spice has shown potential as a natural remedy fora wide range of chronic diseases, such as neurodegenerative disorders, type 2 diabetes,cardiovascular problems, and metabolic sy
*AntiDiabetic↑,
*tau↓, Key compounds in cinnamon, particularly cinnamaldehyde, are believed to protect the brain by inhibiting the aggregation of tau and amyloid-beta (Aβ) proteins, both of which are hallmark features of Alzheimer’s disease.
*Aβ↓,
*antiOx↑, cinnamon’s antioxidant and anti-inflammatory properties help mitigate oxidative stress and inflammation in the brain
*Inflam↓,
*ROS↓, Neurochemicalanalysis showed reduced oxidative stress, evidenced by lower levels of malondialdehyde and nitrites, as well as increased reduced glutathione.
*MDA↓,
*GSH↓,
*cardioP↑, es, has long beenutilized in herbal medicine to support cardiovascular health and treat cardiovascular diseases(CVDs
*LDL↓, Specifically, cinnamon can lower levels of LDL (bad) cholesterol andtriglycerides, while increasing HDL (good) cholester
*HDL↑,
*other↝, particularly beneficial for treatinginflammatory bowel diseases (IBD) such as colitis.
*TNF-α↓, lowering levels of inflammatory markers such as TNF-α, IL-6, and MPO, andby downregulating the expression of TLR-4.
*IL6↓,
*MPO↓,
*TLR4↓,
*GutMicro↑, cinnamon can also support a balanced gut microbiota, which is essential for overall digestive health. By inhibiting the growth of harmful bacteria and fungi, while promoting the growth of beneficial microorganisms
*lipid-P↓, can improve ulcerative colitis (UC) in rats by reducinginflammation, lipid peroxidation, and histological damage
*Wound Healing↑, Combining cinnamon oil(CO) with aloe vera (AV) (COVA) has been shown to effectively inhibit bacterial growth and promote wound healing.
Dose↝, Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon, has garnered attention in pharmacological research due to its diverse therapeutic applications.
TumCP↓, CA and its derivatives have antitumor effects, which encompass inhibiting cell proliferation, arresting the cell cycle, inducing apoptosis, limiting cell migration and invasion, and suppressing angiogenesis.
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
angioG↓,
*Inflam↓, including anti-inflammatory (3), antioxidant (4), antiviral (5), anti-bacterial (6), antithrombic (7), hypoglycemic (8), hepatoprotective (9), anti-diabetic (10), neuroprotective (11) and anticancer effects
*antiOx↑,
*Bacteria↓,
*AntiThr↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
AntiCan↑,
ChemoSen↑, can enhance the effectiveness of anticancer drugs and ensure patient safety.
*BioAv↝, the bioavailability of intravenous administration of CA was superior to that of oral administration
*BioAv↑, A into CA solid lipid nanoparticles, which increased the oral bioavailability of CA by >1.69 times.
eff↑, Especially when combined with hyperthermia therapy at 42°C and 43°C, CA could inhibit cell proliferation
CDK1↓, CB403 (Fig. 1) is a cinnamaldehyde derivative that inhibits the activity of cyclin-dependent kinases (CDKs), particularly CDK1, CDK2 and CDK4, thereby halting cell cycle progression.
CDK2↓,
CDK4↓,
cJun↓, 2-hydroxycinnamaldehyde (HCA; Fig. 1) inhibits the growth of SW620 colon cancer cells by reducing the expression of c-Jun and c-Fos, inhibiting the DNA binding activity of activator protein 1, and inducing cell apoptosis
cFos↓,
Apoptosis↑,
PI3K↓, CA can induce apoptosis in colon cancer cells by inhibiting the PI3K/Akt signaling pathway
Akt↓,
E-cadherin↑, CA upregulates the expression of E-cadherin while downregulating the expression of matrix metalloproteinase-2 (MMP2) and MMP9
MMP2↓,
MMP9↓,
TOP1↓, increases the sensitivity of CRC cells to 5-FU by reducing the expression of thymidylate synthase, ERCC1, DNA topoisomerase 1 and BRCA1
BRCA1↓,
ROS↑, CA was also able to induce apoptosis in cancer cells by increasing intracellular ROS levels
BAX↑, A induces cell apoptosis by upregulating Bax expression, and downregulating Bcl-2 and X-linked inhibitor of apoptosis (XIAP) expression
Bcl-2↓,
XIAP↓,
MMP↓, CA can also induce apoptosis in leukemia K562 cells by reducing the mitochondrial transmembrane potential via mitochondrial-mediated pathways
STAT3↓, figure 2
mTOR↓,
NF-kB↓, ↓NF-κB
eff↑, CA-Cu-PDA was able to release copper ions and CA in tumor cells, and weakened the antioxidant system by binding to glutathione (GSH), which in turn produced additional ROS, thereby inducing enhanced oxidative stress effects
toxicity↓, Consistent with these findings, another study has demonstrated that CA does not exhibit genotoxic or carcinogenic effects on the body
cardioP↑, CA has demonstrated a capacity to alleviate cardiotoxicity induced by DOX
CIT↓, Carica papaya leaf has unique therapeutic and medicinal characteristics against thrombocytopenia, and this is supported by scientific studies.
*Imm↑, therapeutic benefits of the leaf include immunomodulatory, antiviral, antidiabetic, anticancer, antimalarial, antiangiogenic, antibacterial, and antioxidant activities.
*AntiDiabetic↑,
*AntiCan↑,
angioG↓,
*Bacteria↓,
*antiOx↑,
*antiOx↑, contains various chemical compounds demonstrate significant antioxidant properties including caffeic acid, myricetin, rutin, quercetin, α-tocopherol, papain, benzyl isothiocyanate (BiTC), and kaempferol
*ROS↓, it can counteract pro-oxidants via a number of signaling pathways that either promote the expression of antioxidant enzymes or reduce ROS production.
*Inflam↓, Anti-inflammation activities of Carica papaya.
*AntiDiabetic↑, Anti-diabetes activities of Carica papaya
*neuroP↑, fermented papaya preparation (FPP) exerted neuroprotective properties against copper induced neurotoxicity in Swedish mutant human APP (APPsw) cells
*Wound Healing↑, Wound healing activities of Carica papaya.
*GSH↑, Carica papaya peel extract significantly increased glutathione (GSH), while decreasing MDA and ROS production. Thus, preventing DNA damage and induction of colonic carcinogenesis
*MDA↓,
*DNAdam↓,
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cardioP↑, According to modern pharmacological investigations, crocetin possesses cardioprotective, hepatoprotective, neuroprotective, antidepressant, antiviral, anticancer, atherosclerotic, antidiabetic, and memory-enhancing properties.
hepatoP↑,
*neuroP↑,
AntiCan↑,
*AntiDiabetic↑,
*memory↑,
*BioAv↓, poor bioavailability hinders therapeutic applications, derivatization and formulation preparation technologies have broadened the application prospects for crocetin.
*ROS↓, Crocetin can act via different mechanisms, such as enhancing the rate of oxygen transport and diffusivity, inhibiting pro-inflammatory mediators, protecting cells from reactive oxygen species (ROS) damage, and stimulating apoptosis in cancer cells
Apoptosis↑,
*lipid-P↓, Myocardial hypertrophy rats Decreases the LPO content and increases the activities of GSH-Px and SOD
*SOD↑,
SOD↓, MCF-7 cells Crocetin (200 μmol/L) Inhibits SOD activity by affecting copper binding sites
ERα/ESR1↓, MCF-7 cells Crocetin glucosyl ester IC50 from 31.25 to 1,000 μg/ml Inhibits estrogen receptor α and HDAC2 mediated signaling cascade
HDAC2↓,
TumCCA↑, KYSE-150 cells Crocetin (0, 12.5, 25, 50, 100, 200 μmol/L) S-phase cell arrest
Bax:Bcl2↑, AGS cells Crocetin (50–240 μmol/L) Decreases the Bcl-2/Bax ratio of AGS cells
IL6↓, HCT116 cells Crocetin (30 µM) Downregulates inflammation-related genes, HMGB1, IL-6, and IL-8
IL8↓,
Shh↓, Cancer stem cells (CSC) Inhibits the expression of Sonic hedgehog (SHH)
COX2↑, HeLa cells Upregulates COX-2 expression
*GSK‐3β↓, Alzheimer’s disease (AD) SH-SY5Y and PC12 cells Inhibits the active forms of GSK3β and ERK 1/2 kinases and significantly reduces the total tau protein and tau protein phosphorylation
*ERK↓,
*tau↓,
*ROS↓, crocetin-induced inhibition of Aβ1-42-induced hippocampal HT22 cell death could be mediated via reduced ROS production.
*GSTs↑, The activities of antioxidant enzymes [GSH-Px, GSH reductase (GR), GST, CAT, and SOD]
*Catalase↑,
*SOD↑,
*BioAv↑, The bioavailability of crocetin can be improved by formulating a crocetin injection
*Bacteria↓, multiple pharmacological properties such as antibacterial, antifungal, antiparasitic, antineuraminidase, antioxidant, anti-inflammatory, and anticancer activities.
*AntiFungal↑,
*antiOx↑,
*Inflam↓,
AntiCan↑,
*AntiDiabetic↑, also demonstrated an antidiabetic effect, through its role in the prevention of obesity and metabolic problems associated with high-fat diets
*Obesity↓,
TumCCA↑, Anticancer mechanisms of carvone are due to its different actions against checkpoints of cancer cells such as inducing apoptosis and cell cycle arrest
*AntiArt↑, figure 2
Imm↑,
*P450↓, decreased levels of phase I enzymes (cytochrome P450 and cytochrome b5) with increased levels of phase II enzymes (GR, GST, and GSH) and increased expression of Bax, caspase-3, and caspase-9 with decreased expression of mutated p53 and Bcl-2 in anima
*GSR↑,
GSTs↑,
GSH↑,
BAX↑,
Casp3↑,
TumCP↓, Results showed that L-carvone exhibited a strong antiproliferative effect against MCF7 (IC50 = 1.2 mM) and MDA MB 231 cells (IC50 = 1.0 mM), inhibited the migration of breast cancer cell lines, and induced apoptosis.
TumCMig↓,
Apoptosis↑,
*Inflam↓, anti-inflammatory, antioxidant, antimalarial, antimicrobial, hepatoprotective and antitumor potential.
*antiOx↑,
*hepatoP↑,
AntiTum↑,
AntiCan↑, important anticancer/chemopreventive potential
*chemoPv↑,
*AntiDiabetic↑, antidiabetic, hepatoprotective, and immunomodulator
*Imm↑,
Hif1a↓, for gastric cancer, cucurbitacin B reversed the multi-drug resistance of the SGC7901/DDP gastric cancer cells by downregulating the drug-resistant protein HIF-1a and P-pg.
P-gp↓,
mTORC1↓, cucurbitacin B induced apoptosis and autophagy by inhibiting mTORC1.
ERK↓, by inactivating the extracellular signal-regulated kinase (ERK) 1/2, p38, and the Akt signaling pathway [61].
Akt↓,
Casp3↑, substantial increase in the activity of Caspase 3/7 in the human prostate cancer cell lines LNCaP and PC-3,
Casp7↑,
ATP↓, authors proposed cucurbitacin’s dose-dependent inhibition of ATP citrate lyase, or ACYL, as the anticancer mechanism of cucurbitacin, in in vitro and in vivo prostate tumour models
RadioS↑, cucurbitacin B combined with ionizing radiation blocks cancer cells in the G2/M phase and promotes apoptosis, inhibiting cancer cells.
ChemoSen↑, cucurbitacin B exhibited cytotoxicity against the ovarian cancer cell line A2780, and pretreatment of cisplatin-resistant cell line A2780CP with this natural compound led to a significant increase in the cytotoxicity of cisplatin
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*antiOx↑, Date palm products are rich in carbohydrates, dietary fiber, essential minerals, and phenolic and flavonoid compounds, such as gallic acid, catechin, quercetin, and ferulic acid, which underpin their antioxidant and anti-inflammatory properties.
*Inflam↓,
*AntiBio↑, Experimental studies further suggest potential antimicrobial, antihyperlipidemic, antidiabetic, anticancer, anti-arthritic, neuroprotective, hepatoprotective, and gastroprotective effects.
*AntiDiabetic↑,
*AntiCan↑,
*AntiArt↑, biosynthesized AgNPs derived from date seed extracts has been reported to exhibit anti-arthritic activity in experimental models
*neuroP↑,
*hepatoP↑,
*GastroP↑,
*other↝, The mineral composition of date palm fruits (Table 6) reveals potassium as the most abundant mineral, followed by magnesium, calcium, and phosphorus.
*cardioP↑, This mineral profile supports the use of date palm fruit as a functional food for cardiovascular health, particularly in individuals with hypertension, due to its high potassium and low sodium content.
*cognitive↑, Multiple preclinical studies provided evidence that these compounds may enhance brain health and cognitive performance by mitigating oxidative stress and modulating inflammatory mediators, thus alleviating memory impairments and inflammation.
*ROS↓,
*memory↑, reported that date palm extracts were associated with improvements in memory performance, antioxidant enzyme activity, and preservation of neuronal morphology, particularly in the CA1 region of the hippocampus
*other↝, numerous literature have reported that both date fruit and seed extracts may alleviate oxidative stress, subsequently exerting anti-inflammatory, cardioprotective, and metabolic regulatory effects through modulation of related signaling pathways.
*SOD↑, Date fruit extract treatment was also found to restore antioxidant enzyme activities including superoxide dismutase (SOD) and catalase (CAT), and elevated glutathione (GSH) levels, further strengthening its proposed protective role against oxidative
*Catalase↑,
*GSH↑,
*GA↑, rich in phenolic acids and flavonoids, such as gallic acid, catechin, epicatechin, p-coumaric acid, ferulic acid, syringic acid, vanillic acid, quercetin, apigenin, caffeic acid, rutin, and lutein,
*Catechins↑,
*FA↑,
*QC↑,
Api↑,
*CA↑,
*Imm↑, Phoenix dactylifera L. extracts have also been reported to enhance immune function. The high polyphenol content in Phoenix dactylifera L. has been shown to stimulate immune responses
*Phen↑,
*IL1β↓, downregulation of pro-inflammatory mediators, including IL-1β, tumor growth factor (TGF)-β, COX-1, and COX-2, in middle-aged women following chronic consumption of date seed
*TGF-β↓,
*COX1↓,
*COX2↓,
TumCP↓, Phoenix dactylifera L. aqueous-ethanolic extract demonstrated antiproliferative and anti-inflammatory activities against human breast cancer cell lines (MDA-MB-231 and MCF-7)
Casp3↑, seed extracts demonstrated pro-apoptotic effects via caspase-3 activation in MDA‑MB‑231 cells
TumMeta↓, exhibited antiproliferative effects against U87 glioblastoma and MDA‑MB‑231 cells, along with significant inhibition of cell adhesion and migration, indicating potential anti-metastatic properties.
*GutMicro↑, It was suggested that daily consumption of dates may provide fermentable substrates for gut microbiota, thereby reducing toxic protein-derived metabolites.
*other↝, The most common fermented foods and beverages require lactic acid bacteria (LAB), AAB, bacilli or other bacteria, yeasts, or filamentous fungi.
*toxicity↓, Fermented foods that contain appreciable levels of fermentation-produced organic acids (>100 mM), combined with low water activity, salt, nitrite and other antimicrobials, have a long record of food safety78. Likewise, beverages containing 4% or more
*toxicity↓, Food fermentations can also enhance food safety and nutritional quality by removing toxic or anti-nutritive compounds from the raw ingredients.
*Obesity↓, Yoghurt consumption is associated with reductions in adiposity factors (BMI, waist circumference)105, type 2 diabetes mellitus and cardiovascular disease
*AntiDiabetic↑,
*cardioP↑,
*GutMicro↑, including nutritive alteration of raw ingredients and the biosynthesis of bioactive compounds, modification of the human gut microbiota, and development and modification of the immune system
*Imm↑, As approximately 70% of the human immune system is located in the gastrointestinal tract
*GutMicro↑, Alternatively, the high-fermented food diet steadily increased microbiota diversity and decreased inflammatory markers.
*Inflam↓, Fermented food intake decreases markers of host inflammation
*Imm↑, The data highlight how coupling dietary interventions to deep and longitudinal immune and microbiome profiling can provide individualized and population-wide insight.
*Obesity↓, Large cohort studies as well as limited interventional studies have linked the consumption of fermented foods with weight maintenance and decreased diabetes, cancer, and cardiovascular disease risks
*AntiDiabetic↑,
*AntiCan↑,
*cardioP↑,
*IL6↓, inflammatory serum proteins that decreased over the fermented food intervention including IL-6, IL-10, and IL-12b
*IL10↓,
*IL12↓,
*GutMicro↑, Improving the gut microbiome and reducing inflammation through dietary inputs like fermented foods may therefore be a path to improving human health status
*Inflam↓,
*BP↓, figure 2
*LDL↓,
*HDL↑,
*CRP↓,
*IL6↓,
*TNF-α↓,
*Obesity↓,
*AntiDiabetic↑,
*cardioP↑, fermented dairy consumption was associated with a decreased risk of general CVD compared with controls
*GutMicro↑, yogurt consumption also coincided with transient increases in Streptococcus thermophilus and Bifidobacterium animalis subsp. lactis in feces, microbes commonly found in yogurt cultures, suggesting a role for the gut microbiome in mediating effects [
*neuroP↑, Evidence also suggests a potential protective role of fermented foods against age-related neurologic diseases such as dementia and Alzheimer’s disease.
*cognitive↑, 30 participants with Alzheimer’s disease found that daily consumption of 200 mL milk fermented with L. acidophilus, Lacticaseibacillus casei, B. bifidum, and Limosilactobacillus fermentum (2 × 109 CFU/g each) for 12 wk improved mini-mental state exam
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Risk↓, Intermittent fasting (IF) has emerged as a potential adjunctive strategy in cancer prevention, mitigation, and treatment.
TumCMig↓,
IGF-1↓, IF may reduce cancer risk, including its effects on insulin-like growth factor 1 suppression, autophagy induction, and chronic inflammation reduction.
TumAuto↑,
Inflam↓, IF has been shown to reduce chronic inflammation,13,40 a risk factor for various cancers
ChemoSen↑, we discuss IF’s potential to enhance the efficacy of conventional cancer therapies by sensitizing cancer cells, promoting apoptosis, and reducing treatment-related side effects.
Apoptosis↑,
chemoP↑, IF has shown potential in protecting healthy tissues during chemotherapy.
*glucose↓, Fasting has been shown to enhance metabolic health by improving insulin sensitivity, lowering blood sugar levels, and reducing the risk of type 2 diabetes.
*AntiDiabetic↑,
*cardioP↑, Recent studies support the cardioprotective effect of IF by reducing cholesterol levels, lowering blood pressure, and improving cardiovascular health
*LDL↓,
*BP↓,
*neuroP↑, IF may reduce the risk of neurodegenerative diseases, enhance cognitive function, and improve memory
*cognitive↑,
*memory↑,
*OS↑, some studies have suggested that IF may extend lifespan and improve overall health
*QoL↑,
Imm↑, In the context of cancer prevention, IF may directly affect the function of immune cells, reducing their production of inflammatory cytokines and promoting a more anti-inflammatory environment.5
TumCG↓, Evidence suggests that FMDs can effectively slow tumor growth by altering cancer cell metabolism, enhance the efficacy of traditional cancer therapies by reducing side effects, and potentially bolster antitumor immune surveillance
ChemoSideEff↓, IF may also help alleviate common side effects such as fatigue, nausea, and weight loss associated with cancer treatments
QoL↑, Results showed that chemotherapy-induced QoL decline was significantly less pronounced during fasting periods compared to non-fasting periods
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other↑, Limonene is an unparalleled terpenoid with numerous therapeutic benefits.
DDS↑, Incorporating it into sophisticated drug delivery systems and medical devices, together with personalised medicine strategies, signifies notable progress in its therapeutic use.
*antiOx↑, graohical abstract
*Inflam↓,
*AntiDiabetic↑,
*neuroP↑,
*Imm↑,
*Wound Healing↑,
*other↑, Limonene can act as a solvent for cholesterol and has, therefore, been used curatively to dissolve gallstones.
*BioAv↑, orally administered D-limonene shows complete absorption from the GI tract of both animals and humans.9
*ROS↓, thereby preventing the further generation of reactive oxygen species (ROS), as depicted in Figure 2
*SOD↑, D-limonene restored the activities of antioxidant enzymes, such as SOD, CAT, GP, and GSH level, further resulting in the reduction of oxidative stress by preventing DNA damage and protein denaturation. T
*Catalase↑,
*GSH↑,
*DNAdam↓,
*AntiDiabetic↑, D-limonene is found to reduce oxidative stress and induce the potentiation of beta cells in the pancreas, thus showing beneficial effects in diabetes mellitus
Casp3↑, D-limonene activates caspases 3 and 9
Casp9↑,
BAX↑, increases the expression of BAX protein, and decreases BCL2 protein expression,
Bcl-2↓,
*AChE↓, Limonene inhibited AChE and BChE activities by 10% and 12%, respectively.
*BChE↓,
*Aβ↓, Limonene decreased Aβ42-induced neuronal cell death and reduced ROS levels, adversely affecting extracellular signal-regulated kinase (ERK) phosphorylation
*ROS↓,
*toxicity?, D-limonene shows low toxicity effects and has not shown much affirmation in animal studies. Some studies have reported that they are non-carcinogenic in humans and do not show much toxicity, even after several years, when administered at low doses.
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*antiOx↑, spanning antioxidant, anti-inflammatory, antitumor, antidiabetic, neuroprotective, and gastroprotective domains.
AntiTum↑,
*AntiDiabetic↑,
*neuroP↑, The neuroprotective potential of limonene has been demonstrated in different neurodegenerative diseases (NDs), including multiple sclerosis, stroke, epilepsy, Alzheimer’s disease (AD), and anxiety
*GastroP↑,
*ROS↓, we explore its molecular mechanisms, ranging from reactive oxygen species mitigation
*toxicity↓, Its low toxicity and high bioavailability support its potential as a safe adjunct or alternative in phytotherapy.
*BioAv↑,
ChemoSen↑, combining limonene with tamoxifen increases the anticancer efficacy by inducing apoptosis in MCF 7 BC cells
BAX↑, MCF-7 cells, D-limonene treatment significantly increases the expression of Bcl-2-associated X protein (Bax) and p53 while downregulating Bcl-2, inducible nitric oxide synthase (iNOS), and COX-2
P53↓,
Bcl-2↓,
iNOS↓,
COX2↓,
eff↑, IC50 of free limonene was reported to be 985.00 μg/mL, whereas its encapsulation in chitosan nanoparticles (LimChiNPs) significantly reduced the IC50 to 650.70 μg/mL.
ROS↑, Furthermore, this dual therapy augmented intracellular reactive oxygen species production and promoted cell cycle arrest predominantly at the G1 phase via the modulation of cyclin D1 and B1 [20].
TumCCA↑,
cycD1/CCND1↓,
CycB/CCNB1↓,
TumCMig↓, migration capacity of MCF-7 cells was also markedly inhibited under the combined regimen, suggesting potential to curb metastatic progression
*lipid-P↓, Limonene therapy resulted in a decrease in lipid peroxidation levels and an increase in the level of glutathione, a major antioxidant that helps protect cells from damage
*GSH↑,
*SOD↑, Moreover, the activity of antioxidant enzymes (SOD and glutathione peroxidase (GPx)) was improved, indicating that the body’s natural defense system was functioning better again
*GPx↑,
*hepatoP↑, limonene treatment has been shown to mitigate liver damage caused by DEN/2-AAF exposure by reinforcing the antioxidant defenses in hepatic cells
*glucose↓, D-limonene consistently lowered fasting glucose and HbA1c, improved lipid profiles, and enhanced antioxidant defenses (e.g., increased SOD, CAT, and GSH levels)
*AGEs↓, D-limonene has been shown to inhibit the formation of advanced glycation end products (AGEs) through multiple mechanisms,
*Obesity↓, Notably, limonene also stimulates differentiation and glucose uptake in adipocytes, suggesting a role in counteracting insulin resistance and obesity-related metabolic dysfunction
*Aβ↓, The neuroprotective properties of limonene find expression in suppressing Aβ-induced cell death and decreasing ROS levels
*AChE↓, Further insights into the molecular mechanism of limonene’s inhibition of AChE have been provided by molecular dynamics simulations
Dose↝, Key bioactive compounds, such as taraxasterol, chlorogenic acid, chicoric acid, and taraxinic acid, have been identified as promising agents capable of inhibiting tumor cell proliferation and modulating oncogenic pathways.
TumCP↓,
toxicity↓, Given its multi-target biological activity and low toxicity, Taraxacum officinale holds significant potential for integration into oncotherapy as an adjuvant treatment.
*AntiDiabetic↑, reported to exhibit a broad spectrum of pharmacological effects, including antidiabetic, antioxidant, hepatoprotective, diuretic, anti-inflammatory, neuroprotective, antidepressant, antimicrobial, and immunostimulant properties
*antiOx↑,
*hepatoP↑,
*diuretic↑,
*Inflam↓,
*neuroP↑,
*Imm↑,
eff↑, Innovative formulations such as silver nanoparticles synthesized using aqueous leaf extracts (TOL-AgNPs) demonstrated enhanced cytotoxicity, achieving 95% inhibition of HepG2 cell proliferation at 200 μg/mL
Apoptosis↑, Figure 1
tumCV↓,
selectivity↑,
TumCMig↓, taraxasterol inhibits papillary thyroid cancer cell migration and prevents epithelial-mesenchymal transition (EMT) induced by TGF-β by decreasing the expression of matrix metalloproteinases MMP-2 and MMP-9 and blocking the Wnt/β-catenin signaling pa
EMT↓,
MMP2↓,
MMP9↓,
Wnt↓,
β-catenin/ZEB1↓,
PI3K↓, regulation of key signaling pathways such as PI3K/Akt, JNK, and ERK1/2.
Akt↓,
JNK↓,
ERK↓,
*Inflam↓, including anti-inflammatory, anti-tumor, immunostimulatory, anti-microbial, anti-viral, anti-oxidant, anti-diabetic, geno-protective, diuretic and kidney-protective, hepato-protective, neuro-protective
*AntiTum↑,
*Imm↑,
*antiOx↑,
*AntiDiabetic↑,
*diuretic↑,
*RenoP↑,
*hepatoP↑,
*neuroP↑,
AntiTum↑, In 1981, for the first time, it was shown that the hot water extract of dandelion possessed anti-tumor activity
TNF-α↑, It induces apoptotic cell death by raising the production of tumor necrosis factor (TNF)-α and interleukin (IL)-1α
IL1β↑,
Apoptosis↑, The TNF-α and IL-1α are two potent inducers of cancer cell apoptosis
MMP2↓, dampening the activities of matrix metallopro-
teinases (MMPs) such as MMP-2 and MMP-9
MMP9↑,
eff↑, Combination treatment with TRAIL targeting and dandelion resulted in TRAIL-induced apoptosis mediated through inhibition of
the MKK7-TIPRL interaction and subsequent ac-
tivation of MKK7-JNK phosphorylation.
Diff↑, The differentiation-inducing effects of dandelion on the human leukemia cell line (HL60) and a B16 mouse melanoma-derived sub-clone with high differentiation capability (B16 2F2) were investigated
*ROS↓, Both cell viability and ROS assays confirmed that extract effectively attenuated glutamate-induced cytotoxicity and ROS generation.
*HO-1↑, Moreover, extract increased
the expression of HO-1 and promoted the nuclear
translocation of nuclear factor erythroid 2-relat-
ed factor-2 (Nrf2).
*NRF2↑,
*lipid-P↓, andelion can improve lipid metabolism and
is advantageous in preventing diabetic complica-
tions from lipid peroxidation and free radicals in
diabetic rats124
tumCV↓, Several in vitro and in vivo studies have demonstrated the cytotoxic ability of Taraxacum species, which can be possibly explained by the complexity and diversity of its phytochemical profile.
*AntiDiabetic↑, Decoction of the whole plant is traditionally used in Mexico as an antidiabetic (Hernandez-Galicia et al., 2002).
*Imm↑, to enhance immune response to upper respiratory tract infections, bronchitis or pneumonia as well as is used as a compress due its anti-mastopathy activity.
*diuretic↑, These properties are diuretic, hepatoprotective, anticolitis, immunoprotective, antiviral, antifungal, antibacterial, antiarthritic, antidiabetic, antiobesity, antioxidant and anticancer effects
*hepatoP↑,
*Imm↑,
*Bacteria↓,
*AntiArt↑,
*AntiDiabetic↑,
*Obesity↓,
*antiOx↓,
*AntiCan↑,
Dose?, The main phytochemicals are: carotenoids; flavonoids (e.g., quercetin, chrysoeriol, luteolin-7-glucoside); phenolic acids (e.g., caffeic acid, chlorogenic acid, chicoric acid); polysaccharides (e.g., inulin); sesquiterpene lactones (e.g., taraxinic a
AntiCan↑, anticancer, hepatoprotective, antiinflammatory, antioxidant and antimicrobial activities.
*hepatoP↑,
*Inflam↑,
*antiOx↑,
*AntiBio↑,
*BioAv↓, Pharmacokinetic studies have demonstrated that emodin has poor oral bioavailability in rats because of its extensive glucuronidation.
*AntiViral↑, pharmacological effects, such as antiviral, antibacterial, anti‐allergic, anti‐osteoporotic, anti‐diabetic, immunosuppressive, neuroprotective and hepatoprotective activities.
*AntiDiabetic↑,
*neuroP↑,
CSCs↓, Emodin effectively blocked the self‐renewal activity of glioma stem cells by suppressing crucial stemness signalling pathways involving Notch‐1, b‐catenin and STAT3.
NOTCH↓,
β-catenin/ZEB1↓,
STAT3↓,
TumCCA↑, that cells in G2/M phase increased significantly and that the proportion of S‐phase cells gradually declined
*TNF-α↓, inhibiting the serum expression levels of TNF‐α, IL‐6 and IL‐1β
IL6↓,
IL1β↓,
*MMP9↓, emodin treatment effectively inhibited allergen‐induced inflammation by reducing the Th2 immune response, suppressing MMP‐9 expression and inducing HO‐1 expression in a murine model of asthma
*HO-1↑,
cMyc↓, Emodin strongly inhibits the expression of proteins and genes, such as C‐MYC, MCL1, CCND1, CK2, IKK2, PKC, TGF‐β1, Smad4 and Bcl‐2/Bax.
Mcl-1↓,
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve
Showing Research Papers: 1 to 50 of 68
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 68
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CBR1↓, 1, CIT↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, GSH↑, 1, GSTs↑, 1, HO-1↑, 1, lipid-P↑, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 10, ROS↝, 1, SOD↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 2, MEK↓, 1, mitResp↓, 1, MMP↓, 3, mtDam↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, cMyc↓, 3, Glycolysis↓, 2,
Cell Death(tgid=5) ⓘ
Akt↓, 6, p‑Akt↓, 1, Apoptosis↓, 2, Apoptosis↑, 12, BAX↑, 4, Bax:Bcl2↑, 3, Bcl-2↓, 3, Bcl-2↑, 1, Casp1↑, 1, Casp3↑, 8, Casp7↑, 1, Casp9↑, 3, Cyt‑c↑, 1, iNOS↓, 1, JNK↓, 1, MAPK↓, 1, Mcl-1↓, 1, PUMA↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
cJun↓, 1, other↑, 1, other↝, 1, tumCV↓, 5,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↓, 1, TumAuto↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
BRCA1↓, 1, DNAdam↑, 1, P53↓, 1, P53↝, 1, p‑P53↑, 1, PARP↑, 1, PCNA↓, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 2, CDK4↓, 2, CycB/CCNB1↓, 1, cycD1/CCND1↓, 3, P21↑, 1, TumCCA↑, 11,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
cFos↓, 1, CSCs↓, 2, Diff↑, 1, EMT↓, 3, EMT↝, 1, ERK↓, 3, GSK‐3β↓, 1, p‑GSK‐3β↓, 1, HDAC2↓, 1, IGF-1↓, 1, miR-34a↓, 1, mTOR↓, 3, mTORC1↓, 1, NOTCH↓, 2, NOTCH1↓, 1, NOTCH1↑, 1, PI3K↓, 7, Shh↓, 1, STAT3↓, 3, TOP1↓, 1, TRPM7↓, 1, TumCG↓, 5, Wnt↓, 1,
Migration(tgid=13) ⓘ
p‑Cofilin↑, 1, E-cadherin↓, 1, E-cadherin↑, 2, F-actin↓, 1, Ki-67↓, 2, MMP2↓, 6, MMP9↓, 6, MMP9↑, 1, MMPs↓, 3, N-cadherin↓, 1, Slug↓, 1, TET1↑, 1, TRIB3↑, 1, TumCI↓, 5, TumCMig↓, 8, TumCP↓, 5, TumMeta↓, 4, TumMeta↑, 1, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 6, EGFR↓, 1, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 3, VEGF↓, 3,
Barriers & Transport(tgid=15) ⓘ
P-gp↓, 2, P-gp⇅, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, COX2↑, 1, IL1β↓, 1, IL1β↑, 1, IL6↓, 3, IL8↓, 1, Imm↑, 2, Inflam↓, 3, Inflam↝, 1, NF-kB↓, 2, NF-kB↑, 1, NK cell↑, 2, p65↓, 1, TNF-α↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
ERα/ESR1↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 2, BioAv↝, 2, ChemoSen↑, 10, DDS↑, 1, Dose?, 1, Dose↝, 4, eff↓, 1, eff↑, 18, Half-Life↓, 1, RadioS↑, 3, selectivity↑, 3,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, BRCA1↓, 1, EGFR↓, 1, ERα/ESR1↓, 1, IL6↓, 3, Ki-67↓, 2, TG/TAG↓, 1, TRIB3↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 13, AntiDiabetic↑, 2, AntiTum↑, 5, cardioP↑, 3, chemoP↑, 2, chemoPv↑, 2, ChemoSideEff↓, 1, hepatoP↑, 1, neuroP↑, 1, OS↑, 1, QoL↑, 1, Risk↓, 1, Risk↑, 1, toxicity↓, 3,
Ingredients & Constituents(tgid=25) ⓘ
Api↑, 1,
Total Targets: 159
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 4, AntiBio↑, 4, diuretic↑, 3,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 2, antiOx↑, 29, Catalase↑, 8, GPx↑, 8, GSH↓, 1, GSH↑, 8, GSR↑, 2, GSTs↑, 1, HDL↑, 3, HO-1↑, 4, lipid-P↓, 10, MDA↓, 8, MPO↓, 1, NQO1↑, 1, NRF2↑, 7, ROS↓, 25, ROS↑, 1, SOD↑, 13,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, ATP↑, 1, Insulin↑, 2, mtDam↓, 1, OCR↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 3, AMPK↓, 1, AMPK↑, 1, glucose↓, 6, HMG-CoA↓, 1, LDH↓, 3, LDL↓, 6, NAD↓, 1, PFK↓, 1, PPARα↝, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↓, 1, BAX↓, 2, Bcl-2↓, 1, Bcl-2↑, 1, Casp↓, 1, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, Fas↓, 1, GADD34↓, 1, iNOS↓, 2, JNK↓, 1, necrosis↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, other↓, 2, other↑, 3, other↝, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↓, 1, HSP70/HSPA5↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↓, 1, LC3II↓, 1, MitoP↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 4, P53↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, GSK‐3β↓, 3, Nestin↑, 1, NOTCH1↑, 1, PI3K↑, 2, SOX2↑, 1, TRPM7↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 2, AntiAg↑, 6, Ca+2↓, 1, Ki-67↑, 1, MMP9↓, 2, TGF-β↓, 1, TRPC1↓, 1, Tyro3↓, 1, ZO-1↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1, Hif1a↓, 1, NO↓, 1, TXA2↓, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1, GastroP↑, 2, OCLN↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↓, 2, COX2↓, 6, CRP↓, 1, IFN-γ↓, 1, IL10↓, 2, IL10↑, 1, IL12↓, 1, IL17↓, 1, IL1β↓, 3, IL6↓, 7, Imm↓, 1, Imm↑, 15, Inflam↓, 29, Inflam↑, 1, NF-kB↓, 8, PGE2↓, 2, TLR4↓, 2, TNF-α↓, 8,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 7, BChE↓, 3, BDNF↓, 1, BDNF↑, 2, GABA↑, 1, MAOA↓, 1, NGF↑, 1, tau↓, 3, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 2, Aβ↓, 6, BACE↓, 2, MAOB↓, 1, NLRP3↓, 1, PP2A↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CYP19↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 8, BioAv↑, 9, BioAv⇅, 1, BioAv↝, 3, Dose↑, 1, Dose↝, 3, eff↓, 1, eff↑, 5, P450↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 3, ALP↓, 1, AST↓, 5, BP↓, 8, CRP↓, 1, GutMicro↑, 11, IL6↓, 7, Ki-67↑, 1, LDH↓, 3,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 7, AntiDiabetic↑, 49, AntiTum↑, 1, Bone Healing↑, 1, cardioP↑, 21, chemoPv↑, 3, cognitive↑, 7, fatigue↓, 1, hepatoP↑, 21, memory↑, 11, motorD↑, 1, neuroP↓, 1, neuroP↑, 30, Obesity↓, 12, OS↑, 2, Pain↓, 2, QoL↑, 1, RenoP↑, 3, toxicity?, 1, toxicity↓, 6, toxicity↝, 1, toxicity∅, 1, Weight↓, 2, Wound Healing↑, 11,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↓, 1, AntiFungal↑, 4, AntiViral↑, 2, Bacteria↓, 15, Sepsis↓, 1,
Ingredients & Constituents(tgid=25) ⓘ
CA↑, 1, Catechins↑, 1, FA↑, 1, GA↑, 1, Phen↑, 1, QC↑, 1,
Total Targets: 176
Scientific Paper Hit Count for: AntiDiabetic, AntiDiabetic
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1385 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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