AntiViral Cancer Research Results
AntiViral, AntiViral: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Var, |
NA |
|
|
|
*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation
| - |
in-vitro, |
CRC, |
HCT116 |
|
|
|
- |
in-vitro, |
Nor, |
HEK293 |
|
|
|
NRF2↑, Nanosilver increased Nrf2 protein expression and disrupted the cell cycle at the G1 and G2/M phases.
TumCCA↑, AgNPs interact with DNA to stop
the cell cycle and lead to apoptosis
ROS↑, Nanosilver induced significant mitochondrial oxidative stress in HCT116, whereas it did not in the non-cancer HIEC-6 and nanosilver/sodium ascorbate co-treatment was preferentially lethal to HCT116 cells,
selectivity↑,
*AntiViral↑, AgNPs are effective antiviral agents against various viruses such as human
immunodeficiency virus, hepatitis B virus, and monkey pox virus through interaction with
surface glycoproteins on the virus
*toxicity↝, Citrate and PVP-coated AgNPs have been found to be less toxic than non-coated AgNPs
ETC↓, AgNPs affects mitochondrial function through the disruption of the electron transport
chain2,24,26,33,39–41
MMP↓, Studies have shown that exposure to AgNPs resulted in a decrease of mitochondrial membrane potential (MMP) in various in vitro and in vivo experiments
DNAdam↑, AgNPs has also been shown to interact with and induce damage to DNA, DNA strand breaks, DNA damage
Apoptosis↑, apoptosis induced by AgNPs were through membrane lipid peroxidation, ROS, and oxidative stress
lipid-P↑,
other↝, Several studies have showed AgNPs interact with various proteins such as haemoglobin, serum albumin, metallothioneins, copper transporters, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), malate dehydrogenase (MDH), and bacterial proteins.
UPR↑, Studies have shown exposure to AgNPs induces activation of the UPR
*GRP78/BiP↑, AgNPs induced increased levels of GRP78, phosphorylated PERK, phosphorylated eIF2-α, and
phosphorylated IRE1α, spliced XBP1, cleaved ATF-6, CHOP, JNK and caspase 12
*p‑PERK↑,
*cl‑eIF2α↑,
*CHOP↑,
*JNK↑,
Hif1a↓, One study showed AgNPs inhibits HIF-1 accumulation and suppresses expression of HIF-1 target genes in breast cancer cells (MCF-7) and also found the protein
levels of HIF-1α and HIF-1β decreased
AntiCan↑, Many studies have shown that ascorbic acid, on its own, has anti-cancer effects
*toxicity↓, However, when the rats were treated with both ascorbic acid
and AgNPs, a decrease in toxic effects was observed in non-cancer parotid glands in rats
eff↑, Studies have shown both AgNPs and ascorbic acid have greater effects and toxicity in
cancer cells relative to non-cancer cells
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Diabetic, |
NA |
|
|
|
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
*toxicity↓, Chicoric acid is a rare and valuable functional food ingredient with no obvious dose dependence, no overdose side effects, and no contraindications and drug interactions.
*Inflam↓, promising pharmacological effects in regulating glucose and lipid metabolism; anti-inflammatory, antioxidant, and anti-aging properties, and against digestive system diseases
*antiOx↑,
*AntiAge↑,
*eff↝, The amount of chicoric acid is closely related to the plant source, medicinal parts, harvest period, processing, and extraction methods.
*Dose↝, content of chicoric acid in the stems, leaves, and flowers were 9.7%, 44.7%, and 23.6%, respectively
*neuroP↑, neuroprotection effects
*AntiViral↑, its antivirus properties,
*AntiBio↑, Antimicrobial activities for curcumin and rhizome extract of C. longa against different bacteria, viruses, fungi, and parasites have been reported.
*Bacteria↓, These results demonstrated promising antibacterial activity for different curcumin derivatives as well.
*AntiViral↑, Antiviral Activity
*BioAv↓, optimum potential of curcumin is limited because of poor oral bioavailability and insufficient solubility in aqueous solvents leading to poor absorption, fast metabolism, and quick systemic elimination
*Half-Life↓,
*eff↑, Alcoholic extracts from freshly harvested Echinacea purpurea were the strongest, with an 80% reduction of antibiotic treatment days, IRR 0.21 [95% CI 0.15–0.28].
*Imm↑, Echinacea can safely prevent RTIs and associated complications, thereby decreasing the demand for antibiotics.
*AntiViral↑, reported broad-spectrum antiviral effects of alcoholic fresh-plant Echinacea extracts
*antiOx↑, high content of antioxidant and anti-inflammatory substances.
*Inflam↓,
AntiCan↑, anti-cancer effect of EGCG may be related to inhibiting tumour angiogenesis, antioxidant effects and suppressing the inflammatory processes contributing to transformation
Risk↓, Consuming large amounts of EGCG may contribute to reducing the incidence of colorectal cancer, partly due to inhibiting tumour growth factors.
TumCG↓, EGCG is capable of inhibiting growth and inducing apoptosis of cancer cells
Apoptosis↑,
*ROS↓, The main effect of anti-inflammatory and antioxidant substances is to inhibit signalling in the inflammatory process by scavenging ROS
*cardioP↑, EGCG may potentially exert a protective effect on the heart muscle in patients undergoing surgery who are susceptible to ischemic injury,
*Imm↑, The immunomodulatory properties of green tea and its antiviral effect may support the prevention and regulate immune response in infectious diseases, including COVID-19
*AntiViral↑,
*cognitive↑, Consumption of green tea is regarded as an effective dietary intervention to promote clarity of mind and cognitive function.
*antiOx↑, bioactivities of EGCG, including its antioxidant, anti-inflammatory, anticancer, cardiovascular protective, metabolic regulatory, neuroprotective, gut microbiota-modulating, and antimicrobial properties.
*Inflam↓,
*AntiCan↑,
*cardioP↑,
*neuroP↑,
*GutMicro↑,
*AntiBio↑,
*ROS↓, Figure 1, anti inflammatory
*TNF-α↓,
*IL6↓,
TumCP↓,
*LDL↓, cardioprotective
*NO↓,
*Obesity↓, Metabolic syndrome
*p‑tau↓, nervous system
*Aβ↓,
*NRF2↑, , EGCG has been shown to activate the Keap1/P62/Nrf2 signaling pathway,
*SOD↑, upregulation of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, indirectly diminishing the levels of intracellular oxygen free radicals
*Catalase↑,
*GPx↑,
*NLRP3↓, EGCG also restores autophagy levels, suppresses the activation of the NLRP3 inflammasome by inhibiting the mammalian target of rapamycin signaling pathway
*mTOR↓,
TumCCA↑, Cancer: induce cell cycle arrest and inhibit tumor cell proliferation
NRF2↓, EGCG inhibits CCL5-stimulated lung cancer cell proliferation by down-regulating Nrf2 expression
Apoptosis↑, Inducing Apoptosis in Cancer Cells
SIRT1↓, EGCG activates the mitochondrial apoptotic pathway by downregulating SIRT1 expression to modulate the SIRT1-p53 axis
miR-25-5p↓, In breast cancer, EGCG induces apoptosis by inhibiting miR-25 expression and elevating PARP, pre-caspase-3 and pre-caspase-9 protein levels
PARP↑,
Casp3↑,
Casp9↑,
ER Stress↑, in multiple myeloma, EGCG promotes apoptosis by activating the endoplasmic reticulum stress pathway
TumAuto↑, EGCG induces autophagic cell death in breast cancer cells by retaining YAP1 in the cytoplasm and promoting the assembly of the CHMP2B-VPS4B complex
EMT↓, EGCG has been demonstrated to inhibit EMT, invasion, and migration by blocking the TGFβ/Smad signaling pathway
TumCI↓,
TumCMig↓,
TGF-β↓,
Smad1↓,
STAT3↓, EGCG can directly bind to STAT3, reducing nuclear localization and inhibiting the transcription of PLXNC1.
VEGF↓, widely believed that EGCG can block this process by reducing the expression of vascular endothelial growth factor, a key factor in angiogenesis,
angioG↓, The inhibition of angiogenic mimicry by EGCG through the Twist/VE-calmodulin/AKT pathway has also been demonstrated in prostate cancer cells
Imm↑, Acting as an Immunomodulator
EGFR↓, EGCG possesses the ability to interact with EGFR and inhibit activity, strengthening the anticancer evidence for EGCG
*GutMicro↑, EGCG can regulate the balance of gut flora. For example, EGCG can inhibit the growth of harmful bacteria such as Escherichia coli and Salmonella, while promoting the proliferation of probiotics like Bifidobacterium and Lactobacillus
*Bacteria↓, Antibacterial and Antiviral Properties of EGCG
*AntiViral↑,
*BioAv↓, EGCG, its low bioavailability in the human body limits clinical efficacy.
*BioAv↑, Nanotechnology strategy of EGCG.
*eff↑, Co-encapsulation assay of EGCG with quercetin shows that the two synergistically enhanced the antioxidant capacity of EGCG
*BioAv↑, Combining EGCG with resveratrol increases its solubility and significantly improves its absorption in the small intestine.
eff↑, combination of EGCG and curcumin inhibits the activity of metabolic enzymes, reduces the rate of metabolism in the liver and enhances its antitumor efficacy
ChemoSen↑, synergistic effects of EGCG combined with chemotherapeutic agents such as 5-fluorouracil, celecoxib, cisplatin, and tamoxifen have also been reported
*toxicity↝, The European Food Safety Authority notes in scientific opinion that daily oral doses of 800 mg or higher of EGCG represent a common starting point for observed cases of liver injury
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↓,
*antiOx↑, its role as health-promoting effect is attributed because it is rich source of antioxidant.
P53↑, anticancer management through the modulation of various molecular pathways including p53, pTEN, NF-κB, PI3K/Akt, Bcl-2, and VEGF
PTEN↑, figure 2
NF-kB↓,
PI3K↓,
Akt↓,
Bcl-2↓,
VEGF↓,
*Inflam↓, Neem also plays role as anti-inflammatory via regulation of proinflammatory enzyme activities including cyclooxygenase (COX), and lipoxygenase (LOX) enzyme.
*COX2↓,
*5LO↝,
*Wound Healing↑, figure 1
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
*AntiViral↑,
*Bacteria↑,
*AntiBio↑,
*AntiFungal↑,
cMyc↓, figure 2
BAX↓,
IAP1↓, Nimbolide downregulated cell survival proteins, including I-FLICE, cIAP-1, cIAP-2, Bcl-2, Bcl-xL, survivin, and X-linked inhibitor of apoptosis protein, and upregulated the proapoptotic proteins p53 and Bax
IAP2↓,
Bcl-xL↓,
survivin↓,
XIAP↓,
angioG↓, ethanolic fraction of neem leaf (EFNL) treatment effectively inhibited the expression of proangiogenic genes,
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*other↝, Nimbolide is one of the most potent limonoids derived from the flowers and leaves of neem (Azadirachta indica), which is widely used to treat a variety of human diseases.
*Inflam↓, Nimbolide has anti-inflammatory, anti-microbial, and anti-cancer properties, which make it an intriguing compound for research.
AntiCan↑,
*Bacteria↓, pharmacological properties including antimalaria, antibacterial, antiviral, antioxidative, anti-inflammatory, antiinvasive, neuroprotective, hepatoprotective, and pro-apoptotic properties
*AntiViral↑,
*neuroP↑,
*hepatoP↑,
*ROS?, Inhibit oxidative stress, Activate Nrf2/HO-1 signaling
*NRF2↑,
*HO-1↑,
*TLR4↓, Inhibit oxidative stress Anti-inflammatory and antioxidant TLR4/NF-κB signaling pathway
*NF-kB↓,
*AChE↓, down regulation of AChE and Aβ GSK-3β interaction
*Aβ↓,
*GSK‐3β↓,
*LDL↓, Nimbolide reduced intracellular cholesterol, free fatty acids, and triglycerides and enhanced hepatocyte function by inhibiting oxidative DNA damage and lipid peroxidation through its antioxidant effects
*DNAdam↓,
*lipid-P↓,
*antiOx↑, Nimbolide showed immense antioxidant properties.
*SOD1↑, nimbolide treatment increased superoxide dismutase (SOD-1), Nrf-2, GSH, and HO-1 protein expression
*GSH↑,
*IL6↓, Nimbolide treatment resulted in a reduction of the inflammatory cytokines IL-6, IL-1β, and TNF-α, as well as inflammatory cellular signaling molecules IkB-α, STAT3, and NF-kB.
*IL1β↓,
*STAT3↓,
*GPx↑, Glutathione peroxidase, catalase (CAT), concentration were all found to be up, while malondialdehyde and nitric oxide levels were shown to be significantly reduced by nimbolide.
*Catalase↑,
*MDA↓,
*AntiDiabetic↑, Anti-diabetic effect of nimbolide in diabetes
*HDL↓, suppression of the levels of pro-inflammatory mediators, (cholesterol, TG, LDL, and HDL, MCP-1, VEGF, and MMP-9)
*MCP1↓,
*VEGF↓,
*MMP9↓,
*GutMicro↑, nimbolide showed to reduce inflammation, oxidative stress, and to reverse gut microbiota, which protects them from gestational diabetes.
TumCP↓, Nimbolide reported to decrease cell proliferation, EMT, cell cycle progression, and migration, in breast cancer cells via downregulating the NF-κB pathway
TumCCA↑,
TumCMig↓,
NF-kB↓,
ROS↑, nimbolide stimulates the overproduction of ROS, consequently modulating both autophagy and apoptosis in pancreatic cancer cells.
PI3K↓, nimbolide-induced ROS generation hindered cell proliferation by suppressing PI3K/AKT/mTOR and ERK signaling pathways.
Akt↓,
mTOR↓,
ERK↓,
EMT↓, nimbolide-mediated ROS generation reduced EMT, migration, colony forming abilities and invasion, thereby inhibiting metastasis.
TumMeta↓,
ChemoSen↑, use of nimbolide in combination with 5-FU showed a higher inhibitory rate in breast cancer than 5-FU alone
eff↑, nimbolide synergized the effect of TRAIL to induce apoptosis in tumor cell lines, but not normal breast cells
selectivity↑,
CDK4↓, slows tumor growth by inhibiting CDK4/6 activity
CDK6↓,
Wnt↓, nimbolide suppressed the Wnt/β-catenin signaling pathway mediated by NF-κB in HCC and pancreatic cancer cells
β-catenin/ZEB1↓,
STAT3↓, nimbolide can significantly suppress the activation of oncogenic transcription factor STAT3.
MMP2↓, inhibits tumor cell growth and migration by downregulating VEGF-A and MMP-2/9 expression,
Sp1/3/4↓, nimbolide inhibited MMP-9 activity by inhibiting the binding activity of Sp-1, AP-1 and NFk-B motifs, all of which are important transcription factors.
AP-1↓,
P21↑, Nimbolide exhibited dose-dependent inhibitory effects on HeLa cell viability by causing cell cycle arrest at G0/G1 phase with p53-dependent accumulation of p21.
*AntiArt↑, The findings of the study suggest that nimbolide has the ability to reduce the severity of rheumatoid arthritis by suppressing the expression levels of toll-like receptors, IL-23, IL-17, IFN-γ and HSP70.
*IL23↓,
*IL17↓,
*IFN-γ↓,
*HSP70/HSPA5↓,
*AntiBio↑, TQ, have a broad antimicrobial spectrum including Gram-negative, Gram-positive bacteria, viruses, parasites, schistosoma and fungi.
*AntiViral↑,
*AntiFungal↑,
Inflam↓, Ursolic acid has been shown to target multiple proinflammatory transcription factors, cell cycle proteins, growth factors, kinases, cytokines, chemokines, adhesion molecules, and inflammatory enzymes.
TumCCA↑,
chemoPv↑, potentially mediate the chemopreventive and therapeutic effects of ursolic acid by inhibiting the initiation, promotion and metastasis of cancer.
TumMeta↓,
antiOx↑, Numerous biochemical and pharmacological effects of ursolic acid, including anti-inflammatory, antioxidant, antiproliferative, anticancer, antimutagenic, antiartherosclerotic, antihypertensive, antileukemic, antiviral, and antidiabetic, have been rep
AntiViral↑,
AntiDiabetic↑,
Showing Research Papers: 1 to 14 of 14
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, lipid-P↑, 2, MFN2↑, 1, NRF2↓, 1, NRF2↑, 1, ROS↑, 4,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, ETC↓, 1, MMP↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
cMyc↓, 2, SIRT1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 4, Apoptosis↑, 4, BAX↓, 1, BAX↑, 1, Bcl-2↓, 1, Bcl-xL↓, 1, Casp3↑, 1, cl‑Casp3⇅, 1, Casp9↑, 2, Cyt‑c↑, 2, IAP1↓, 1, IAP2↓, 1, JNK↓, 1, MAPK↝, 1, Mcl-1↓, 1, p38↑, 1, survivin↓, 2,
Kinase & Signal Transduction(tgid=6) ⓘ
miR-25-5p↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 2, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 3, P53↑, 2, P53↝, 1, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 1, P21↑, 1, TumCCA↑, 7,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, EMT↓, 2, ERK↓, 1, GSK‐3β↑, 1, mTOR↓, 1, mTOR↝, 1, NOTCH↓, 1, PI3K↓, 3, PTEN↑, 1, STAT3↓, 3, TumCG↓, 1, Wnt↓, 2,
Migration(tgid=13) ⓘ
AP-1↓, 1, fascin↓, 1, MMP2↓, 1, MMP9↓, 1, MMPs↓, 1, Smad1↓, 1, TGF-β↓, 2, TumCI↓, 1, TumCMig↓, 2, TumCP↓, 3, TumMeta↓, 3, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EGFR↓, 1, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 1, VEGF↓, 3,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, IL1β↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 1, NF-kB↓, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 2, Dose↝, 1, eff↑, 10, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 4, AntiDiabetic↑, 1, chemoPv↑, 1, Risk↓, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1,
Total Targets: 92
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiBio↑, 6, TRPA1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 7, Catalase↑, 3, GPx↑, 3, GSH↑, 1, HDL↓, 1, HO-1↑, 3, lipid-P↓, 3, MDA↓, 2, NRF2↑, 3, ROS?, 1, ROS↓, 3, SOD↑, 2, SOD1↑, 1, TAC↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
glucose↓, 1, LDL↓, 2, NADPH↑, 1, PPARγ↓, 1,
Cell Death(tgid=5) ⓘ
JNK↑, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↑, 1, cl‑eIF2α↑, 1, GRP78/BiP↑, 1, HSP70/HSPA5↓, 1, p‑PERK↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, GSK‐3β↓, 3, mTOR↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
5LO↝, 1, MMP9↓, 2, VCAM-1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 2, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 3,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, ICAM-1↓, 1, IFN-γ↓, 1, IL17↓, 1, IL1β↓, 3, IL23↓, 1, IL4↓, 1, IL6↓, 4, Imm↑, 3, Inflam↓, 8, Inflam↑, 1, MCP1↓, 1, MUC2↓, 1, NF-kB↓, 3, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 3,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 1, tau↓, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 3, BACE↓, 1, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 5, Dose↝, 1, eff↑, 4, eff↝, 1, Half-Life↓, 1, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
GutMicro↑, 3, IL6↓, 4, MUC19↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 4, Bone Healing↑, 1, cardioP↑, 3, cognitive↑, 1, hepatoP↑, 3, neuroP↑, 7, Obesity↓, 1, toxicity↓, 3, toxicity↝, 2, Wound Healing↑, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 5, AntiViral↑, 13, Bacteria↓, 5, Bacteria↑, 1,
Total Targets: 90
Scientific Paper Hit Count for: AntiViral, AntiViral
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#:1381 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
Home Page