AntiArt Cancer Research Results
AntiArt, AntiArthritis: Click to Expand ⟱
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Scientific Papers found: Click to Expand⟱
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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].
*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↑,
tumCV↓, D-Carvone treatment suppressed the viability of Molt-4 cells and the IC50 was determined at 20 µM/ml.
ROS↑, The D-Carvone treatment was increased the oxidative stress and reduced the level of antioxidants in the Molt-4 cell lines.
antiOx↓,
MMP↓, diminished MMP was noted in the D-Carvone treatment.
Apoptosis↑, induced the apoptosis in a time and dose dependent manner by the activation of caspases-8, -9 and -3.
Casp8↑,
Casp9↑,
Casp3↑,
*neuroP↑, D-carvone also possessed the neuroprotective [18], anticancer [19,20], antiarthritis [21], and anti-ulcerative colitis [22] activities.
AntiCan↑,
*AntiArt↑,
TBARS↑, We found an augmented level of TBARS and decreased status of SOD, GSH and CAT enzymes in the D-carvone (15 and 20 µM/ml) treated Molt-4 cells when compared to control cells.
SOD↓,
GSH↓,
Catalase↓,
*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
AntiArt↑, this species has been traditionally employed for the treatment of toothache, bowel pain, snake bite, skin disorders, seizure, chronic arthritis, and cancer
*Imm↑, The immunostimulant activity of the plant or its preparations is caused by three mechanisms:
*Neut↑, activation of the neutrophils, macrophages, polymorphonuclear leukocytes (PMN), and natural killer (NK) cells.[
*NK cell↑,
*COX1↓, This effect may be attributed to the inhibition of COX‑1 and to a lesser extent COX‑2 by alkamides.
*COX2↓,
*Inflam↓, The Echinacea preparation, interestingly, has reversed the inflammation caused by some bacteria in a culture of epithelial cells by reducing cytokines
TumCG↑, The extract of the flowers and cichoric acid inhibited both the human colon cancer cell lines Caco‑2 and HCT‑116 in a dose dependent manner after 48 h.
*toxicity↓, Generally, animal studies of various preparations of Echinacea species have shown low toxicity.
*Inflam↓, The wide range of eugenol activities includes antimicrobial, anti-inflammatory, analgesic and antioxidant.
*antiOx↑,
*NF-kB↓, Eugenol also has an inhibitory effect on cell proliferation via suppression of NF-Kappa B (NF-kB).
*AntiArt↑, eugenol may have recovery effects on arthritis and can be useful as a beneficial supplement in the treatment of arthritis.
*lipid-P↓, Eugenol has prevented depression by decreasing the lipid peroxidation and stimulating reduced glutathione (GSH).25
*GSH↑,
ROS↑, The cytotoxic effects of eugenol, induction of reactive oxygen species (ROS) production and reduced levels of GSH have been studied in human submandibular cell line.
GSH↓,
ChemoSen↑, The combination of eugenol and gemcitabine resulted in a decrease in cell viability of 84% (eugenol alone) to 47% (combination of eugenol-gemcitabine).
Apoptosis↑, Furthermore, eugenol has been found to induce apoptosis by destruction the mitochondrial membrane potential and production of reactive oxygen species.38
MMP↓,
TumCG↓, Eugenol showed different degrees of cytotoxicity in HL-60 cancer cells and inhibited the cell growth by 50% at a concentration of 23.7 µM.
TumCCA↑, eugenol arrests cells in the S phase of the cell cycle and induces apoptosis by this function.
Dose↝, Eugenol, a significant bioactive compound, is found in cloves and other traditional Indian medicinal plants, such as cinnamon, tulsi, ginger, turmeric, and Japanese star anise, which have been reported to have significant anticancer properties.
AntiCan↑,
*Inflam↓, also exhibits different pharmacological effects (anti-inflammatory, cardio-protection, and neuroprotection).
*cardioP↑,
*neuroP↑,
angioG↓, eugenol exhibits anti-apoptotic, anti-angiogenic, and anti-metastatic properties in cancer cell lines and in vivo animal models, which we discuss in this review.
TumMeta↓,
*BioAv↑, Oral administration of eugenol promoted rapid absorption by different organs and metabolism in the liver. encapsulation is required to address the issues of early absorption, increased water solubility, and improved efficiency
*eff↑, Eugenol encapsulation as an inclusion with β-cyclodextrin, chitosan, and 2-hydroxypropyl-β-cyclodextrin nanoparticles improves its thermal stability
*toxicity↝, Eugenol at lower doses displayed minimal adverse effects, including contact dermatitis, local irritation, and rare allergic responses. However, at its higher doses, it can lead to liver and kidney damage, tissue injury, sudden onset of seizures, and
antiNeop↑, exhibit antineoplastic properties against different cancers by triggering cell cycle arrest and apoptosis in cancer cells
TumCCA↑,
Apoptosis↑,
*antiOx↑, Eugenol exhibits its antioxidant property due to its unique structural configuration, specifically the presence of an allyl group, as revealed by electron spin resonance
*lipid-P↓, Eugenol prevents lipid peroxidation (Nagababu and Lakshmaiah 1994), hexanal oxidation (Lee and Shibamoto 2001), copper-dependent LDL oxidation, and nonenzymatic peroxidation in liver mitochondria
*ROS↓, Eugenol exhibited 58–81 % DPPH radical scavenging potential in its 0.25–1.0 µM/ml concentration
*SOD↑, Eugenol protects against oxidative damage by increasing the levels of certain antioxidant enzymes, such as SOD, CAT, GST, and GPx (Huang et al. 2015).
*Catalase↑,
*GSTs↑,
*GPx↑,
*iNOS↓, Eugenol pre-treatment increased the levels of antioxidant enzymes and decreased the expression of iNOS, COX2, IL-6, and tumor necrosis factor-α (TNF-α) (Kaur et al. 2010).
*COX2↓,
*IL6↓,
*TNF-α↓,
*AntiArt↑, Administration of eugenol at 33 mg/kg dose in arthritis-induced male Sprague-Dawley rats decreased the swelling of paws and joints (
*Bacteria↓, Along with cinnamaldehyde and thymol, Li et al. determined eugenol's antibacterial activity against E. coli and S. aureus.
TumAuto↑, eugenol activated apoptosis and autophagy through the PI3K/AKT/FOXO3a pathway in cancer cells(breast cancer cells).
PI3K↓, PI3K/Akt/mTOR pathway inhibition
Akt↓,
FOXO3↝,
BAX↑,
mTOR↓, PI3K/Akt/mTOR pathway inhibition
NF-kB↓, NF-κB signaling pathway inhibition
P53↑, In some cancers, eugenol has been shown to upregulate p53, thereby inhibiting cancer growth.
TumCG↓,
CSCs↓, eugenol downregulated certain signaling cascades of the Wnt signaling pathway and specific cancer stem cell markers, including CD44, EpCAM, Notch1, and Oct4, in breast cancer cell lines treated with eugenol.
CD44↓,
EpCAM↓,
NOTCH1↓,
OCT4↓,
Bcl-2↓, Eugenol also downregulates the protein expressions of p85, BCL-2, PDK1, HER2, AKT, BAD, Cyclin D1, and NF-KB.
PDK1↓,
HER2/EBBR2↓,
BAD↓,
cycD1/CCND1↓,
ROS↑, EUG-medium chain triglyceride nanoemulsions Liver cancer HB8065 cells Increased the levels of ROS generation to initiated the apoptotic cell death
Casp3↑, apoptosis initiated by Caspase-3
protein upregulation
selectivity↑, Eugenol was not cytotoxic to MCF10A cells; however, it displayed cytotoxic activity in the transformed MCF10A cells (MCF10A-ras).
MMP2↓, A significant decline in matrix metalloproteinase (MMP-2, MMP-9) levels and an increase in tissue inhibitor of metalloproteinase-1 (TIMP-1) expression were also observed.
MMP9↓,
TIMP1↑,
VEGF↓, Eugenol also inhibits metastatic invasion and angiogenesis, as evident from the downregulation of MMP-2, MMP-9, VEGF, and VEGFR1, along with the upregulation of RECK and TIMP-2
VEGFR1↓,
RECK↑,
TIMP2↑,
DNAdam↑, Eugenol demonstrated an apoptosis-inducing effect in HL-60 cells, as evidenced by DNA fragmentation and a DNA ladder assay.
MMP↓, It is accompanied by a decline in mitochondrial membrane potential and thiol levels, early disruption of the lipid layer, DNA fragmentation, and activation of proapoptotic markers (Caspase-3, PARP, p53)
Thiols↓,
PARP↑,
*Pain↓, eugenol nanoemulsion may significantly reduce pain-associated arteriovenous fistula (AVF)
E2Fs↓, t interferes with several critical cancer signaling pathways, including the Wnt/b-Catenin pathway, PI3K/AKT pathway, MAPK/ERK pathway, E2F1/survivin pathway, JNK/STAT3 pathway, and NF-κB signaling pathway, among others.
survivin↓, cause E2F1/survivin downregulation, which activates apoptosis in breast cancer cells
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*AntiCan↑, (Eug), a volatile phenolic bioactive compound with a formula of C10H12O2, has been reported to have anticancer, antidiabetic, cardio‐ and pulmonary protective roles.
*AntiDiabetic↑,
*cardioP↑, Eugenol has been proven effective in modulating gut microbiota and attenuating adiposity in high‐fat diet‐fed C57BL/6J mice.
*toxicity↝, According to WHO, the safe dose of eugenol is 2.5 mg/kg for consumption
*GutMicro↑,
*neuroP↑, Moreover, it has the ability to improve gut health and prevent neurodegenerative disorders.
*BioAv⇅, Furthermore, multiple carriers like liposomes, glycodendritic polyamine dextran, solid lipid nanoparticles, and corn protein nanoparticles have been reported to deliver eugenol.
*BioAv↝, Eugenol (150 mg) in gelatin capsules was orally administered in healthy adults and absorbed very quickly, and ~55% is eliminated in urine after being transformed to glucuronic acid or eugenol sulfate conjugate in the liver
*antiOx↑, The studies on eugenol have proved its antioxidant and anti‐inflammatory properties.
*Inflam↑,
*AntiArt↑, aMateen et al. (2019) reported that eugenol alleviated arthritis via attenuating pro‐inflammatory cytokines (TNF‐α, IL‐6, IL‐10).
*TNF-α↓,
*IL6↓,
*IL10↓,
*GSH↑, Eugenol (2.5, 5, 10 mg/kg) improved GSH, GPx, and CAT levels while reducing carrageenan‐induced OS in arthritic rats (Adefegha et al. 2019).
*GPx↑,
*Catalase↑,
*MDA↓, reported reduced MDA and improved SOD, CAT, and TAC levels.
*TAC↑,
TumCMig↓, eugenol subdued cell migration and invasion by suppressing angiogenesis‐related protein expression and modulating JAK2/STAT3 pathways.
TumCI↓,
Akt↑, MDA‐MB‐231, SK‐BR‐3 ↑AKT, FOXO3a, Caspase‐3/9, p21
FOXO3↑,
Casp3↑,
Casp9↑,
P21↑,
angioG↓, Eugenol has been reported to reduce angiogenesis, inhibit invasion, and trigger apoptosis
TumCI↓,
Apoptosis↑,
NF-kB↓, GC via apoptosis induction, metastasis inhibition, downregulation of NF‐κB, and angiogenesis reduction is shown in Figure 3
eff↑, eugenol (153 μM) combined with 5‐fluorouracil proved effective in inhibiting cell growth and division in HeLa cells.
eff↑, eugenol (200–350 μM) with sulforaphane (6.5–8 μM) lowered the expressions of COX‐2, IL‐β, and Bcl‐2 and inhibited cell proliferation
ChemoSen↑, co‐treatment of eugenol and cisplatin reduced cell proliferation and induced apoptosis in G361 melanoma cells via inhibited MMP and proteasome activity,
NA↑, Eugenol proved effective in HL‐60 cell lines by inducing ROS‐mediated apoptosis with a 23.7 IC50 value
Casp3↑, eugenol‐induced apoptosis via ROS production and caspase‐9/3 activation.
Casp9↑,
*AntiDiabetic↑, Chilukoti et al. (2024) verified the antidiabetic activity of eugenol in rats.
*glucose↓, eugenol (400 mg/kg) significantly lowered glucose levels, reduced OS and inflammation, inhibited MDA levels, and improved GSH.
*ROS↓,
*Inflam↓,
*MDA↓,
*GSH↑,
*BioAv↑, Multiple delivery systems, such as liposomes, nanoparticles, nanoemulsions, and hydrogels, enhance its bioavailability, controlled release, and targeted delivery, making eugenol more effective for pharmaceutical and biomedical applications.
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*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↓,
Showing Research Papers: 1 to 9 of 9
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned ⓘ
AntiArt↑, 1, CBR1↓, 1, NA↑, 1,
Redox & Oxidative Stress ⓘ
antiOx↓, 1, Catalase↓, 1, GSH↓, 2, GSH↑, 1, GSTs↑, 1, ROS↑, 5, SOD↓, 1, TBARS↑, 1, Thiols↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 3,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, PDK1↓, 1,
Cell Death ⓘ
Akt↓, 2, Akt↑, 1, Apoptosis↑, 6, BAD↓, 1, BAX↑, 2, Bax:Bcl2↑, 1, Bcl-2↓, 1, Casp3↑, 5, Casp8↑, 1, Casp9↑, 3, PUMA↑, 1, survivin↓, 1,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
tumCV↓, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 2,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 1, PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 1, E2Fs↓, 1, P21↑, 2, TumCCA↑, 5,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 1, CSCs↓, 1, EMT↓, 1, EpCAM↓, 1, ERK↓, 1, FOXO3↑, 1, FOXO3↝, 1, mTOR↓, 2, NOTCH1↓, 1, NOTCH1↑, 1, OCT4↓, 1, PI3K↓, 2, STAT3↓, 1, TumCG↓, 2, TumCG↑, 1, Wnt↓, 1,
Migration ⓘ
AP-1↓, 1, Ki-67↓, 1, MMP2↓, 2, MMP9↓, 2, RECK↑, 1, TET1↑, 1, TIMP1↑, 1, TIMP2↑, 1, TumCI↓, 2, TumCMig↓, 3, TumCP↓, 2, TumMeta↓, 2, VEGFR1↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 3, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
Imm↑, 1, Inflam↓, 1, NF-kB↓, 3,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, ChemoSen↑, 5, Dose?, 1, Dose↝, 1, eff↑, 7, Half-Life↓, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers ⓘ
HER2/EBBR2↓, 1, Ki-67↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 4, antiNeop↑, 1,
Total Targets: 87
Pathway results for Effect on Normal Cells:
NA, unassigned ⓘ
AntiArt↑, 8, diuretic↑, 1,
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 5, Catalase↑, 3, GPx↑, 3, GSH↑, 4, GSR↑, 1, GSTs↑, 1, HDL↓, 1, HO-1↑, 1, lipid-P↓, 3, MDA↓, 3, NRF2↑, 1, ROS?, 1, ROS↓, 3, SOD↑, 1, SOD1↑, 1, TAC↑, 1,
Core Metabolism/Glycolysis ⓘ
glucose↓, 1, LDL↓, 1,
Cell Death ⓘ
iNOS↓, 1,
Transcription & Epigenetics ⓘ
other↝, 1,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↓, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 2,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 1, STAT3↓, 1,
Migration ⓘ
MMP9↓, 1,
Angiogenesis & Vasculature ⓘ
VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 2, IFN-γ↓, 1, IL10↓, 1, IL17↓, 1, IL1β↓, 1, IL23↓, 1, IL6↓, 3, Imm↑, 2, Inflam↓, 6, Inflam↑, 1, MCP1↓, 1, Neut↑, 1, NF-kB↓, 2, NK cell↑, 1, TLR4↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, BDNF↑, 1, GABA↑, 1,
Protein Aggregation ⓘ
AGEs↓, 1, Aβ↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↑, 2, BioAv⇅, 1, BioAv↝, 1, eff↑, 2, P450↓, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 2, IL6↓, 3,
Functional Outcomes ⓘ
AntiCan↑, 2, AntiDiabetic↑, 6, cardioP↑, 3, hepatoP↑, 3, memory↑, 1, neuroP↑, 5, Obesity↓, 2, Pain↓, 1, RenoP↑, 1, toxicity↓, 1, toxicity↝, 2,
Infection & Microbiome ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 4,
Total Targets: 72
Scientific Paper Hit Count for: AntiArt, AntiArthritis
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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