Obesity Cancer Research Results
Obesity, Obesity: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
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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.
*NRF2↑, CA and CS themselves are not electrophilic, but in response to oxidation, become electrophilic, and then activate the Keap1/Nrf2/ARE (antioxidant response element)
*GSH↑, EP3s dramatically increase GSH levels by transcriptional upregulation of the enzyme’s synthetic machinery via Nrf2 activation.
*neuroP↑, neuroprotective diterpene-type PEDs such as CA and CS
*Inflam↓, CA and CS have been reported to display beneficial effects against acute and chronic inflammation, cardiovascular diseases, obesity, and cancer [94, 95],
*cardioP↑,
*Obesity↓,
*angioG↓, antiangiogenesis [99], protection against cisplatin [100], induction of neurotrophins [101], protection in an Alzheimer’s disease model [102], inhibition of NF-κB
chemoP↑,
*NF-kB↓,
*antiOx↑, antioxidant (8), anti-inflammatory (9) and anti-obesity (10) properties.
*Inflam↓,
*Obesity↓,
chemoPv↑, Many laboratories have reported that capsaicin possesses chemopreventive and chemotherapeutic effects
Apoptosis↑, Capsaicin has been shown to induce apoptosis in many different types of cancer cell lines including pancreatic (19) colonic (24), prostatic (25), liver (26), esophagieal (27), bladder (28), skin (29), leukemia (30), lung (31), and endothelial cells (
selectivity↑,
TRPV1↑, Transient receptor potential vanilloids (TRPVs) are receptors of capsaicin which lead to Ca2+-mediated mitochondrial damage and cytochrome c release.
Ca+2↑,
mtDam↑,
Cyt‑c↑,
P53↑, Capsaicin was found to induce p53 phosphorylation at the Ser-15 residue (30) and enhanced p53 acetylation through down-regulation of sirtuin 1 (
SIRT1↓,
TumCCA↑, Capsaicin induced G0/G1 phase arrest in human esophageal carcinoma cells with an increase of p21 and a decrease of CDK4, CDK6 and cyclin E (
P21↑,
CDK4↓,
CDK6↓,
cycE/CCNE↓,
angioG↓, Capsaicin has anti-angiogenic properties both in vitro and in vivo
TumMeta↓, Capsaicin treatment significantly reduced the metastatic burden in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice (57).
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*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein
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Obesity↓, Capsaicin can also promote weight loss, making it potentially useful for treating obesity.
Half-Life↓, The clinical usefulness of capsaicin is limited by its short half-life.
antiOx↑, Capsaicin exerts analgesic, antioxidant, cardioprotective, anticancer and thermogenic effects, and it can promote weight loss
TRPV1↑, (TRPV1), to which capsaicin binds specifically.
STAT3↓, capsaicin may inhibit signal transducer and activator of transcription 3 (STAT3), but the minimal concentration needed to inhibit STAT3 (50 M) is substantially higher than the concentration required to stimulate TRPV1 (1–5 M)
Ca+2↑, mechanisms appear to involve accumulation of intracellular Ca2+, generation of reactive oxygen species, disruption of mitochondrial membrane potential and upregulation of the transcription factors NF-κB and STATS.
ROS↑,
MMP↓,
*neuroP↑, Capsaicin has demonstrated therapeutic potential in several animal models of Alzheimer's disease (AD).
*tau↓, capsaicin substantially ameliorated synaptic damage and tau hyperphosphorylation induced by cold water stress.
*Inflam↓, capsaicin appeared to activate TRPV1 in M1/M2 dopaminergic neurons, which may alleviate neuro-inflammation and oxidative stress from activated glia
*ROS?,
*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↓,
*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.
*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
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*Aβ↓, chlorogenic acid can reduce Aβ plaques in Alzheimer’s disease model mice by 37%, indicating its neuroprotective potential.
*neuroP↑,
*cardioP↑, Similarly, CGAs offer protection to the cardiovascular system, gastrointestinal tract, kidneys, and liver, while additionally preventing metabolic syndrome and displaying anticancer and antimicrobial capabilities.
*GastroP↑,
*RenoP↑,
*hepatoP↑,
*Obesity↓,
*Bacteria↓,
*BioAv↑, hydroxycinnamoyl-CoA quinate hydroxycinnamoyl transferase, HQT in tomatoes significantly enhances CGA accumulation without significantly altering the levels of other soluble phenolic botanical drugs.
*BioAv↑, Mechanistic studies have shown that dietary fats (such as soybean oil and coconut oil) can significantly enhance the permeability of CGA in the Caco-2 monolayer by increasing cell membrane fluidity
*BioAv↑, Following oral administration of CGA, the acidic environment in the stomach helps maintain the structural stability of CGA, with approximately one-third of the dose entering the blood system through passive diffusion in the small intestine, while the
*ROS↓, CGA pretreatment markedly diminished ROS caused by PD toxins
*GutMicro↑, CGA works with the gut microbiota and its metabolites to alleviate post-infectious irritable bowel syndrome (PI-IBS)
*IBI↑, CGA increases intestinal damage repair, decreases MCT-1 and TFF-3 expression, and suppresses NF-κB expression
*MCT1↓,
*NF-kB↓,
*DNMT1↓, Liver Cancer, DNMT1 protein expression↓
*Imm↑, Chitosan is capable to stimulate immune responses.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was synthesized.
eff↑, GC was designed for immune stimulations in combination with phototherapies in the treatment of metastatic tumors.
*toxicity↓, No toxic effects of GC were observed in cultured cells or in animal studies. I
*TNF-α↑, immunological effect of GC was investigated through its stimulation of TNFα secretion by macrophages in vitro.
*Obesity↓, a dietary supplement for weight loss
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TumVol↓, chitosan-based nanoparticles reduced tumors (doxorubicin (DOX) + survivin siRNA and curcumin + siRNA).
toxicity↓, Their initial studies reveal low toxicity and long-term medication delivery.
Half-Life↑,
eff↑, that allows drug release in reductive cellular environments (especially cancer cells with elevated glutathione levels),
selectivity↑, This clever nanocarrier reacts to intracellular cues and delivers its therapeutic payload mostly to cancer cells while protecting healthy tissues
Dose↝, These co-delivery systems take advantage of chitosan's mucoadhesive properties and protection against enzymatic degradation, enabling oral or nasal administration routes that traditionally pose challenges for peptide delivery
*BDNF↑, Chitosan nanoparticles delivering a combination of brain-derived neurotrophic factor (BDNF) protein and Nrf2 plasmid DNA have been shown to support synaptic plasticity, inhibit oxidative stress, and slow neurodegeneration.
*NRF2↑,
*ROS↓,
*neuroP↑,
*memory↑, In preclinical trials, such strategies improved memory retention, cognitive performance, and neuronal survival in rodent models
*cognitive↑,
*Obesity↓, obese non-human primates illustrated how chitosan-based codelivery of metformin and fibroblast growth factor 21 (FGF21) plasmid DNA targeted adipose tissue to achieve a 40 % reduction in visceral fat
AGEs↓, Chitosan that can help reduce AGE (advanced glycation endproducts) levels in patients with prostate cancer.
Wound Healing↑, Chitosan is approved by the FDA for use in wound dressings
Obesity↓, been used in published clinical trials for weight loss but is not approved for the purposes of this study.
*antiOx↑, wide range of beneficial effects, including antioxidant, antimutagenic, antigenotoxic, anti-cancer, and anti-obesogenic activities.
*toxicity↓, Dietary supplements containing chlorophyll and chlorophyllin are available and generally considered safe, with no reported adverse side effects over several decades of human use
*BioAv↓, Due to the poor bioavailability and stability of chlorophylls, studies on chlorophylls are scarce until now.
*BioAv↑, Semi-synthetic sodium copper-chlorophyllins (SCC) . modifications enhance the stability, solubility in water, and accessibility of SCC
*neuroP↑, figure 3
*Obesity↓,
*AntiCan↑, rats subjected to dietary heme, which mimics red meat ingestion, demonstrated that natural chlorophylls inhibit colonic cytotoxicity, proliferation of colonic epithelial cells, epithelial cell turnover, and the formation of lipid radicals induced by
*TumCP↓, SCC has been reported to decrease the proliferation of human pancreatic cancer cell lines in vitro
*PhotoS↑, Chlorophyll acts as a photosensitizer due to its natural ability to absorb light.
*neuroP↑, chlorophyll may exert its neuroprotective effects is through its antioxidant properties. Oxidative stress
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*toxicity↓, Unlike what happens in other mammals -pets- included, theobromine is safe for humans and has fewer unwanted effects than caffeine
*eff↑, Theobromine, which is found in higher amounts than caffeine, seems to be behind several effects attributed to cocoa intake.
*Half-Life↑, Half-life of theobromine is higher than caffeine even in rodents, which have a faster hepatic metabolism. The mean half-life in plasma from healthy volunteers is approximately 10 h
*eff↑, Theobromine is useful in asthma and in other respiratory tract problems such as cough for which no definitive drug has been developed.
*Inflam↓, Benefits of the theobromine on cough seem to be related with its anti-inflammatory potential as well as with modulation of airway reactivity
*HDL↑, The results of the clinical trial NCT01481389 (clinicaltrials.org) suggest that theobromine but not flavonoids is the responsible for the increase in HDL levels in individuals taking cocoa products
*Obesity↓, theobromine has been considered useful for weight loss and it is supplemented to herbal tea preparations
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*lipid-P↓, inhibition of lipid peroxidation and the protection of LDL-cholesterol against oxidation, and increase resistance to oxidative stress.
*ROS↓,
*Inflam↓, decreasing platelet function and inflammation along with diastolic and systolic arterial pressures, which, taken together, may reduce the risk of cardiovascular mortality.
*BP↓,
*cardioP↑, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*chemoPv↑, They also have antiproliferative, antimutagenic, and chemoprotective effects, in addition to their anticariogenic effects.
*BioAv⇅, great controversy surrounding the bioavailability of phenolics in general and of cocoa derivatives in particular.
*antiOx↑, Cocoa has more phenolics and higher antioxidant capacity than green tea, black tea, or red wine
*Risk↓, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*5LO↓, cocoa polyphenols decrease the plasma concentration of proinflammatory cysteinyl leukotrienes through inhibition of 5-LOX, as demonstrated by Sies et al.
*AntiAg↑, Moreover, cocoa decreases not only platelet aggregation, but also adhesion. 234 mg cocoa phenolics a day for 28 days
*Imm↑, Kenny et al. [21] demonstrated that cocoa oligomers are potent stimulators of both the innate immune system and early events in adaptive immunity.
*NF-kB↓, nd their dimeric forms were found to inhibit the NF-κB activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in T cells,
*other↓, in vivo and in vitro models have provided evidence that pure polyphenols and natural polyphenol plant extracts can modulate intestinal inflammation.
CYP1A1↓, polyphenol cocoa extract leads to the induction of CYP1A1 in breast cancer cells.
COX2↓, hey also inhibited the expression of COX-2,
*Obesity↓, Ferrazzano et al. hypothesized that the polyphenols contained in cocoa may have antiobesity effects due to their ability to suppress fatty acid synthesis while stimulating cell energy expenditure in the mitochondria
*cognitive↑, Moreover, cocoa consumption may also have beneficial effects on satiety, cognitive function, and mood [93].
*BioEnh↑, Firstly, the pre-emulsification of an oil with vegetable lecithin has been shown to increase the systemic bioavailability of certain fatty acids, without increasing total plasma lipid concentrations.
*antiOx↑, different lecithin from various sources (soy, rapeseed) or with differing PL compositions have been reported to exert varying antioxidant properties
*BioEnh↑, ported higher plasma alpha-linolenic acid (ALA) concentrations in the PL-emulsified group
*LDL↓, oybean PL in patients with primary hyperlipidemia has been reported to significantly reduce blood cholesterol levels
*HDL∅, while maintaining plasmatic HDL levels
*Obesity↓, potential of lecithin on the prevention and amelioration of obesity-related metabolic disorders
eff↑, lecithin derived from olive oil compared to that of other seed oils (sunflower, corn or soybean) as a platelet aggregation factor (PAF) antagonist
GutMicro↝, importance of gut microbiota on lipid metabolism and metabolic health renders obligatory that further research on the effect of vegetable lecithin on TMAO production and gut microbiota in general be explored.
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*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol
*Obesity↓, These findings indicate that Vitamin C can reduce obesity-associated cellular stress and thus provide a rationale for future investigations.
*ER Stress↓, Vitamin C prevented the increase in hypoxia (Fig. 1A–B), significantly reduced the induction of ER stress
*Inflam↓, nd ameliorated the increased expression of inflammatory genes
Hif1a↓, Vitamin C treatment for 24 and 48 h significantly reducing induction of HIF1α protein by 30–40% and VEGFA and GLUT1 mRNA by 40–80%
VEGF↓,
GLUT1↓,
GRP78/BiP↓, significantly reversing the effects of TNFα+PA pre-treatment only on GRP78 induction, by 30–40%
Showing Research Papers: 1 to 19 of 19
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, CYP1A1↓, 1, H2O2↑, 1, lipid-P↑, 1, NADH↓, 1, ROS↑, 5, i-ROS↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, MMP↓, 5, MPT↑, 1, mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, SIRT1↓, 2,
Cell Death ⓘ
p‑Akt↓, 1, APAF1↑, 1, Apoptosis↓, 1, Apoptosis↑, 4, BAX↑, 2, Bcl-2↓, 1, Bcl-2↑, 1, Casp↑, 1, Casp1↑, 1, Casp3↑, 2, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 3, p38↑, 1, TRPV1↑, 2,
Protein Folding & ER Stress ⓘ
GRP78/BiP↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 2, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, P21↑, 2, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 2, GSK‐3β↓, 1, mTOR↓, 1, NOTCH↓, 1, PI3K↓, 2, STAT3↓, 1, TOP1↓, 1, TOP2↓, 1, TumCG↓, 1,
Migration ⓘ
Ca+2↑, 4, E-cadherin↓, 1, MMP2↓, 3, MMP9↓, 3, MMPs↓, 1, PKCδ↓, 1, TRIB3↑, 1, TumCMig↓, 2, TumCP↓, 1, TumMeta↓, 2, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, Hif1a↓, 2, VEGF↓, 2,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL6↓, 1,
Protein Aggregation ⓘ
AGEs↓, 1,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↝, 2, ChemoSen↑, 2, Dose↝, 1, eff↑, 4, Half-Life↓, 1, Half-Life↑, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers ⓘ
ALAT↓, 1, EGFR↓, 1, GutMicro↝, 1, IL6↓, 1, TRIB3↑, 1,
Functional Outcomes ⓘ
AntiTum↑, 1, chemoP↑, 3, chemoPv↑, 1, hepatoP↑, 1, Obesity↓, 3, radioP↑, 1, RenoP↑, 1, toxicity↓, 1, TumVol↓, 1, Wound Healing↑, 1,
Total Targets: 90
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 10, Catalase↑, 3, GPx↑, 5, GSH↑, 2, GSR↑, 1, GSTs↑, 1, H2O2↓, 1, HDL↑, 2, HDL∅, 1, lipid-P↓, 3, MDA↓, 3, NADH↓, 1, NRF2↑, 4, RNS↓, 1, ROS?, 1, ROS↓, 9, SOD↑, 5,
Core Metabolism/Glycolysis ⓘ
HMG-CoA↓, 1, LDH↓, 1, LDL↓, 2,
Cell Death ⓘ
Fas↓, 1, MCT1↓, 1, necrosis↓, 1, TRPV1↑, 1,
Transcription & Epigenetics ⓘ
other↓, 2, other↑, 2, PhotoS↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1,
DNA Damage & Repair ⓘ
DNMT1↓, 1,
Proliferation, Differentiation & Cell State ⓘ
TRPM7↓, 1,
Migration ⓘ
5LO↓, 1, AntiAg↑, 5, Ca+2↑, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, NO↓, 1, VEGF↓, 1,
Barriers & Transport ⓘ
BBB↓, 1, GastroP↑, 2, IBI↑, 1, OCLN↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 3, Imm↑, 4, Inflam↓, 12, NF-kB↓, 6, TNF-α↑, 1,
Synaptic & Neurotransmission ⓘ
AChE↓, 2, BChE↓, 1, BDNF↑, 1, tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 2, BACE↓, 1, NLRP3↓, 1,
Hormonal & Nuclear Receptors ⓘ
CYP19↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 5, BioAv↑, 8, BioAv⇅, 1, BioAv↝, 2, BioEnh↑, 2, Dose↝, 2, eff↑, 3, Half-Life↓, 1, Half-Life↑, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
ALP↓, 1, AST↓, 2, BP↓, 3, GutMicro↑, 4, LDH↓, 1, NOS2↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, AntiDiabetic↑, 6, cardioP↑, 10, chemoPv↑, 1, cognitive↑, 3, hepatoP↑, 5, memory↑, 2, motorD↑, 1, neuroP↑, 12, Obesity↓, 16, OS↑, 1, Pain↓, 2, RenoP↑, 2, Risk↓, 1, toxicity↓, 5, Wound Healing↑, 1,
Infection & Microbiome ⓘ
Bacteria↓, 6,
Total Targets: 88
Scientific Paper Hit Count for: Obesity, Obesity
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
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