IL17 Cancer Research Results
IL17, Interleukin-17: Click to Expand ⟱
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Also known as IL-17A.
Interleukin-17A is a protein that in humans is encoded by the IL17A gene.
Higher levels of serum IL-17 are associated with poor prognosis for a variety of solid tumors in cancer patients.
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Scientific Papers found: Click to Expand⟱
Inflam↓, betulinic acid as a promissory lead compound with anti-inflammatory activity
*NO↓, BA can inhibit the production of NO, mainly in macrophages cultures stimulated with bacterial lipopolysaccharide (LPS) and/or interferon gamma (IFN-ɣ)
*IL10↑, (BA) has a broad-spectrum anti-inflammatory activity, significantly increasing IL-10 production, decreasing ICAM-1, VCAM-1, and E-selectin expression and inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB),
*ICAM-1↓,
*VCAM-1↓,
*E-sel↓,
*NF-kB↓,
*IKKα↓, BA blocks the NF-κB signaling pathway by inhibiting IκB phosphorylation and d
*COX2↓, BA also inhibits cyclooxygenase-2 (COX-2) activity and, therefore, decrease prostaglandin E2 (PGE2) synthesis
*PGE2↓,
*IL1β↓, The production of critical pro-inflammatory cytokines, such as IL-1β, IL-6, IL-8, IL-12, and TNF, is also decreased by BA treatment
*IL6↓,
*IL8↓,
*IL12↓,
*TNF-α↑,
*HO-1↑, induction of HO-1 enzyme activity is associated with the anti-inflammatory effect of BA, since SnPP, an inhibitor of HO-1, promoted a partial reversal of BA’s effect on NF-κB activity,
*IL10↑, BA also increased the amount of IL-10, a well-known anti-inflammatory cytokine
*IL2↓, decreasing the production of pro-inflammatory cytokines, such as IL-2, IL-6, IL-17, and IFN-γ
*IL17↓,
*IFN-γ↓,
*SOD↑, BA decreased the production of the inflammatory mediators described above at the inflammation site and increased enzyme activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GRd) in the liver
*GPx↑,
*GSR↑,
*MDA↓, BA decreased malondialdehyde (MDA) levels, a key mediator of oxidative stress and widely used as a marker of free radical mediated lipid peroxidation injury, at the inflammation site
*MAPK↓, BA downregulates MAPK signaling pathways (ERK1/2, JNK, and p38) in the paw edema tissue, which, in part, explains the inhibition of cytokine production (IL-1β and TNF), COX-2 expression, and PGE2 production (Figure 3).
*Inflam↓, brusatol exhibits remarkable anti-inflammatory efficacy in murine models with ulcerative colitis, significantly diminishing serum levels of pro-inflammatory cytokines (e.g., IL-17 and TNF-α), inhibiting IL-22/STAT3 pathway activation,
*IL17↓,
*TNF-α↓,
*IL22↓,
*STAT3↓,
*other↝, brusatol holds promising therapeutic potential in regulating psoriasis with dyslipidemia.
*eff↑, Brusatol significantly reverses the protein profile in IMQ-induced psoriasiform skin lesions
*Dose?, treatment group (Bru) administered brusatol (9.2 mg/kg) via oral gavage for seven consecutive days.
*ROS↓, AB significantly decreased mucous gland hypertrophy, eosinophil infiltration, and oxidative stress marker levels in the allergic airway inflammation-induced AB-pretreated rats.
*Inflam↓, AB pretreatment significantly reduced the levels of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-8, IL-17, monocyte chemoattractant protein-1, C-X-C chemokine receptor type 4 (CXCR4), and thymic stromal lymphopoietin, which were i
*IL1β↓,
*IL6↓,
*IL8↓,
*IL17↓,
*CXCR4↓,
*COX2↓, transcription of cyclooxygenase-2, tumor necrosis factor-α, CXCR4, toll-like receptor 4, Eotaxin-1, and regulated upon activation normal T cell expressed and secreted were significantly suppressed in allergic airway inflammation-induced AB-pretreated
*TLR4↓,
*NO↓, NO, PCO, MDA, and XO, all of these oxidative stress parameters were significantly attenuated in AB-treated allergic airway inflammation-induced rat pups
*MDA↓,
*XO↓,
GutMicro↑, Butyrate, a short-chain fatty acid, is generated through gut microbial fermentation of dietary fiber.
*Inflam↓, Butyrate, a primary anti-inflammatory SCFA, exhibits a multifaceted role in mitigating inflammation
*IL6↓, It inhibits the production of pro-inflammatory cytokines and chemokines, such as IL-6, TNF-α and IL-17, which helps to prevent colon cancer
*TNF-α↓,
*IL17↓,
*IL10↑, while promoting IL-10 production
*ROS↝, regulates the production of reactive oxygen species (ROS)
COX2↓, butyrate has been observed to suppress inflammation by inhibiting the expression of cyclooxygenase-2 mRNA in colonic tissues (60).
NLRP3↓, butyrate exhibits the highest efficiency in the negative regulation of NLRP3
Imm↑, Enhancement of the immunotherapeutic effect
HDAC↓, Inhibition of HDAC activity in cells
TumCCA↑, Butyrate has been found to induce cell cycle arrest in the G0/G1 phase in a dose-dependent manner in vitro in numerous tumors, including colon, liver, lung and bladder cancer,
Apoptosis↑, butyrate-induced apoptosis is accompanied by elevated ROS levels and caspase activity (126)
ROS↑,
Casp↑,
mtDam↑, suggests that ROS can induce mitochondrial membrane damage, release Cyt c from damaged mitochondria, and enhance apoptosis via the Cyt c/caspase-3 pathway
Cyt‑c↑,
eff↑, Clostridium butyricum is an anaerobic bacterium classified as a probiotic due to its production of butyric acid (139)
chemoP↑, butyrate not only alleviates the side effects associated with conventional chemotherapeutic agents such as oxaliplatin, irinotecan and 5-fluorouracil (149-151), but it also enhances the efficacy of both chemotherapy and immunotherapy
ChemoSen↑,
eff↑, metformin has been demonstrated to enhance the biosynthesis of butyrate while concurrently inhibiting the progression of CRC
RadioS↑, Butyrate significantly enhanced radiation-induced cell death and enhanced treatment effects compared with administration of radiation alone.
HCAR2↑, Activation of cell-surface receptors (GPR41, GPR43 and GPR109A);
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*other↝, The most abundant and promising bioactive compound derived from the root of this plant is celastrol, also called tripterine, which possess a broad range of biological activities
*other↝, TW is generally used in the treatment of Crohn’s disease (CD) in China.
*CRP↓, Inflammatory parameters, including c-reactive protein (CRP), also decreased
*eff↝, Etanercept plus TW had an equivalent therapeutic effect to that of Etanercept plus MTX and were both well tolerated
*other↑, TW in human kidney transplantation (26). Rejection occurred in 4.1% of patients treated with TW versus 24.5% of control patients, showing efficacy in the prevention of renal allograph rejection
*CXCR4↓, celastrol decreases hypoxia-induced FLS invasion by inhibiting HIF-1α-mediated CXCR4 transcription
*IL1β↓, Authors have shown that it decreases the production of IL-1β, IL-6, IL-17, IL-18, and TNF by SIC cells harvested from arthritic rats
*IL6↓,
*IL17↓,
*IL18↓,
*TNF-α↓,
*MMP9↓, celastrol reduces MMP-9 production, which limits bone damage
*PGE2↓, celastrol suppresses LPS-induced expression of PEG2 via the downregulation of COX-1 and COX-2 activation
*COX1↓,
*COX2↓,
*PI3K↓, associated with a decrease in PI3K/Akt pathway
*Akt↓,
*other↑, Remarkably, this bone-protective property of celastrol in arthritic models is further supported by studies performed in cancer models
TumCCA↑, celastrol induces cell cycle arrest, apoptosis, and autophagy by the activation of reactive oxygen species (ROS)/c-Jun N-terminal kinases (JNK) signaling pathway
Apoptosis↑,
ROS↑,
JNK↑,
TumAuto↑, celastrol is still able to induce autophagy through HIF/BNIP3 activation
Hif1a↓, The inhibitory effect of celastrol on angiogenesis is mediated by the suppression of HIF-1α,
BNIP3↝,
HSP90↓, The inhibition of HSP90 by celastrol
Fas↑, activation of Fas/Fas ligand pathway in non-small-cell lung cancer
FasL↑,
ETC↓, inhibition of mitochondrial respiratory chain (MRC) complex I
VEGF↓, This inhibition of HIF-1α leads to the decrease of its target genes, such as the VEGF
angioG↓, Angiogenesis Inhibition
RadioS↑, celastrol can overcome tumor resistance to radiotherapy in prostate (129) and lung cancer cells
*neuroP↑, celastrol is a promising neuroprotective agent in animal models of neurodegenerative diseases, such as Parkinson disease (149), Huntington disease (149–151), Alzheimer disease
*HSP70/HSPA5↑, his induction of HSP70 by celastrol explains its beneficial effects not only in neurodegenerative disorders but also in inflammatory diseases.
*ROS↓, celastrol protects human dopaminergic cells from injury and apoptosis and prevents ROS generation and mitochondrial membrane potential loss
*MMP↑,
*Cyt‑c↓, It inhibits cytochrome c release, Bax/Bcl-2 alterations, caspase-9/3 activation, and p38 MAPK activation
*Casp3↓,
*Casp9↓,
*MAPK↓,
*Dose⇅, Authors discuss that it seems to have a narrow therapeutic window, and suggest that it may have a biphasic effect with protective properties at low concentrations and toxic effects at higher concentrations.
*HSPs↑, induces a set of HSPs (HSP27, 32, and 70) in rat cerebral cortical cultures, which are selectively impacted during the progression of this disease
BioAv↓, Due to this poor water solubility, celastrol has low bioavailability. oral administration of celastrol in rats results in ineffective absorption into the systemic circulation, with an absolute bioavailability of 17.06%
Dose↝, narrow therapeutic window of dose together with the occurrence of adverse effects. Our own data showed in vivo that the doses of 2.5 and 5 μg/g/day are effective and non-toxic in the treatment of arthritis in rats;
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*neuroP↑, chrysin has protective effects against neurological conditions by modulating oxidative stress, inflammation, and apoptosis in animal models.
*ROS↓,
*Inflam↓,
*Apoptosis↓,
*IL1β↓, attenuated IL-1β and TNF-α, COX-2, iNOS, and NF-kB expression, activated JNK
*TNF-α↓,
*COX2↓,
*iNOS↓,
*NF-kB↓,
*JNK↓,
*HDAC↓, alleviated histone deacetylase (HDCA) activity, GSK-3β levels, IFNγ, IL-17,
*GSK‐3β↓,
*IFN-γ↓,
*IL17↓,
*GSH↑, increased GSH levels
*NRF2↑, Park's: Increased Nrf2, modulated HO-1, SOD, CAT, decreased MDA, inhibited NF-κB and iNOS
*HO-1↑, upregulated expression of hallmark antioxidant enzymes, including HO-1, SOD, and CAT; and decreased levels of MDA
*SOD↑,
*MDA↓,
*NO↓, Attenuated NO, increased GPx
*GPx↑,
*TBARS↓, decreased levels of TBARS, AChE, restored activities of GR, GSH, SOD, CAT and Vitamin C
*AChE↓,
*GR↑,
*Catalase↑,
*VitC↑,
*memory↑, attenuated memory impairment
*lipid-P↓, attenuated lipid peroxidation
*ROS↓, attenuated ROS
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.
*Imm↑, Fermented foods containing probiotic bacteria and fungi can enhance the immune system, improve gastrointestinal health, and lower the risk of developing various inflammatory diseases.
*GastroP↑,
*Inflam↓,
AntiCan↑, Kombucha tea possesses anticancer, antimicrobial, and hepatoprotective properties
*AntiBio↑,
*hepatoP↑,
*CD4+↑, Kombucha consumption also reduced inflammation by increasing polarization of CD4+ T cells (by induction of IL-4 and TGF-β) and by inhibiting IFN-γ and IL-17
*IFN-γ↓,
*IL17↓,
*GutMicro↑, Kombucha intake also promoted the growth of butyrate-producing bacteria in the gut that exert anti-inflammatory effects
*antiOx↑, fermented turmeric demonstrated stronger antioxidative activity than raw turmeric.
*AST↓, After 5 days of fermentation with Bacillus natto, fermented turmeric dramatically decreased the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in contrast to unfermented turmeric.
*ALAT↓,
*HDL↑, After fermentation, there was a considerable rise in HDL cholesterol and a significant decrease in LDL cholesterol [45].
*LDL↓,
*ROS↓, Kimchi has also demonstrated potent radical scavenging and antioxidant activity in vitro, enhancing LLC-PK1 cell viability by protection against lipid peroxidation.
*lipid-P↓,
*Inflam↓, The anti-inflammatory properties of sauerkraut LAB were emphasized in a randomized, double-blinded pilot study on 34 Norwegian inflammatory bowel syndrome (IBS) patients.
*Aβ↓, Mice fed with doenjang-infused high-fat feed had reduced β-amyloid peptide (Aβ) and neuroinflammatory gene levels, further reinforcing the protective effect of fermented soy on the aging brain
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve
*Inflam↓, Our studies included herein confirm anti-inflammatory effects of PEMF on MSCs and MΦ
*IL1↓, PEMF significantly decreased the production of proinflammatory signaling in IL-1b, IL-6, and IL-17A cytokines (Figs. 1 and 2) in the MSCs.
*IL6↓,
IL17↓,
*TNF-α↓, After exposure to PEMF, outcomes show decreases in the proinflammatory cytokines secretion (IL-1b, IL-6, and TNF-α) and increase/stabilization of IL-10 in THP-1s (
BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,
*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α↓,
*Treg lymp↓, increasing the proportion of Treg cells
*IFN-γ↓, However, on day 20 after immunization, IFN-γ and IL-17A levels in the serum of EAE mice were significantly reduced by the exposure of RMF
*IL17↓,
*CXCc↓, mRNA expression of IFN chemokines (CXCL-1 and CXCL-2), and IL-17 chemokines (CXCL-9 and CXCL-10) had also significantly reduced in EAE mice after RMF exposure.
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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↓,
*other↓, inhibited T cell proliferation in a dose-dependent manner without affecting T cell viability.
*CD25+↓,
*IFN-γ↓,
*IL2↓,
*IL4↓,
*IL17↓,
*CD69↓,
*CTLA-4↓,
*p‑ERK↓,
*IKKα↓,
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ROS↑, In this study, we demonstrated that piperlongumine (PPL) treatment effectively abrogated the hyperproliferation and differentiation of keratinocytes by inducing ROS-mediated late apoptosis with loss of mitochondrial membrane potential.
Apoptosis↑,
MMP↓,
TumCCA↑, the arrest of cell cycle was found at Sub-G1 phase as a result of DNA fragmentation.
DNAdam↑,
STAT3↓, inhibition of STAT3 and Akt signaling was observed
Akt↓,
PCNA↓, decrease in proliferative markers such as PCNA, ki67, and Cyclin D1 along with anti-apoptotic Bcl-2 protein expression
Ki-67↓,
cycD1/CCND1↓,
Bcl-2↓,
K17↓, Keratin 17 is a critical regulator of keratinocyte differentiation, and it was found to be downregulated with PPL significantly
HDAC↓, PPL epigenetically inhibited histone-modifying enzymes, which include histone deacetylases (HDACs) of class I (HDAC1–4) and class II (HDAC6)
ROS↑, PPL at 5 and 10 µM concentration increased the reactive oxygen species (ROS) levels and a marked increase in oxidative stress were observed when combined with H2O2
*IL1β↓, Topical IMQ prominently induced the levels of pro-inflammatory cytokines, including IL-1β, IL-6, TNF-α, IL-17, IL-22, and transforming growth factor (TGF)-β, while PPL significantly suppressed these levels
*IL6↓,
*TNF-α↓,
*IL17↓,
*IL22↓,
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*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells
*Inflam↓, anti-inflammatory, anti-microbial, and anti-proliferative agent.
*eff↑, shown promise in clinical trials for treatment of acne, psoriasis, eczema, common warts, and molluscum contagiosum.
*5LO↓, The oil inhibits the oxidative enzyme 5-lipoxygenase and has DPPH radical scavenging activity and,
*DPPH↓,
*hepatoP↑, in vivo, SAO was able to protect mouse livers from damage resulting from oxidative stress and the formation of reactive oxygen species.
*ROS↓,
*PGE2↓, Production of PGE2 was also suppressed, suggesting that SAO might be acting, at least in part, through inhibition of cyclooxygenase
*IL1β↓, The oil also suppressed the expression of the pro-inflammatory cytokine, IL-1b, in keratinocytes and reduced irritant dermatitis in mouse skin stimulated with haptens.
*IL17↓, reduce levels of IL-17 and the activity of PDE4.
*PDE4↓,
*tyrosinase↓, Alpha-santalol was found to be an inhibitor of tyrosinase, a key enzyme in the biosynthetic pathway for the skin pigment melanin.
*AntiFungal↑, SAO has demonstrated potent activity against many fungal dermatophytes and yeasts including Trichophyton, Microsporum and Candida
angioG↓, alpha-santalol, the primary component of SAO, is anti-angiogenic and inhibits the growth of hepatocellular carcinoma and prostate tumors in vitro and in vivo.
TumCG↓,
DNAdam↑, MCF-7) and non-tumorigenic epithelial breast cells (MCF-10A).42 The authors demonstrated that the oil induced deoxyribonucleic acid (DNA) strand breaks in both cell lines.
*Snail↑, SAO enhanced expression of transcription factors (snail, twist) and mesenchymal factor (vimentin), all of which are related to the epithelial-mesenchymal transition (EMT).
*Twist↑,
*Vim↑,
*EMT↓,
*toxicity↓, other species of sandalwood, such as Western Australian (Santalum spicatum) or Hawaiian sandalwood (Santalum paniculatum), contain significant percentages of farnesol, an irritant, that is not found in oil from S. album.
Apoptosis?, shikonin induced apoptosis and autophagy in RA-FLSs by activating the production of reactive oxygen species (ROS) and inhibiting intracellular ATP levels, glycolysis-related proteins, and the PI3K-AKT-mTOR signaling pathway.
TumAuto↑,
ROS↑,
ATP↓,
Glycolysis↓, shikonin can inhibit RA-glycolysis in FLSs
PI3K↓,
Akt↓,
mTOR↓,
*Apoptosis↓, Shikonin can significantly reduce the expression of apoptosis-related proteins, paw swelling in rat arthritic tissues, and the levels of inflammatory factors in peripheral blood, such as TNF-α, IL-6, IL-8, IL-10, IL-17A, and IL-1β while showing less
*Inflam↓,
*TNF-α↓,
*IL6↓,
*IL8↓,
*IL10↓,
*IL17↓,
*hepatoP↑, while showing less toxicity to the liver and kidney.
*RenoP↑,
PKM2↓, The expression of glycogen proteins PKM2, GLUT1, and HK2 decreased with increasing concentrations of shikonin
GLUT1↓,
HK2↓,
| - |
in-vitro, |
PSA, |
HaCaT |
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- |
in-vivo, |
NA, |
NA |
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*eff↑, SHK treatment significantly improved imiquimod (IMQ)-induced psoriasis symptoms in mice
*IL6↓, attenuated the production of inflammatory cytokines, including interleukin (IL)-6, IL-17, and tumor necrosis factor-alpha (i.e., TNF-α)
*IL17↓,
*TNF-α↓,
*lipid-P↑, enhancing intracellular and mitochondrial ferrous and lipid peroxidation levels
*NRF2↓, by regulating expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear receptor coactivator 4 (NCOA4) and glutathione peroxidase 4 (GPX4)
*HO-1↝,
*NCOA4↝,
*GPx4↓, low dose SHK on LPS inhibited GPX4 and Nrf2 expression
*Ferroptosis↓, inhibited ferroptosis in psoriatic skin by reducing inflammation, ameliorating oxidative stress and iron accumulation.
*Inflam↓,
*ROS↓,
*Iron↓,
Dose↝, India: ar-turmerone 16.7–25.7%, α-turmerone 30.1–32.0%, β-turmerone 14.7–18.4%
Casp3↑, Ar-turmerone has been shown to induce apoptosis in human lymphoma and lymphoblast cells through the activation of caspase-3
MMP9↓, ar-turmerone significantly inhibits the TPA-induced upregulation of MMP-9 and COX-2 expression in human breast cancer cells, effectively blocking critical signaling pathways such as NF-kB, PI3K/Akt, and ERK1/2
COX2↓,
NF-kB↓,
PI3K↓,
Akt↓,
ERK↓,
Inflam↓, Ar-turmerone also mitigates skin inflammation by lowering the levels of TNF-α and IL-6 while downregulating the mRNA synthesis of IL-17, IL-22, and IL-23.
TNF-α↓,
IL6↓,
IL17↓,
IL22↓,
IL23↓,
Inflam↓, anti-inflammatory effect of UA was linked to attenuation of production of proinflammatory cytokines including tumor necrosis factor α, interleukin (IL)-6 and/or IL-17 (
TNF-α↓,
IL6↓,
IL17↓,
NF-kB↓, UA was associated with suppression of the nuclear factor-κB (NF-κβ) pathway, inhibition of expression of cyclooxygenase-2 (COX-2)
COX2↓,
*AntiDiabetic↑, UA demonstrated an antidiabetic functio
*hepatoP↑, UA can provide hepatoprotective activity against several liver diseases
ALAT↓, UA reduced the serum/plasma levels of alanine transaminase and aspartate transaminase, which are liver disease biomarkers
AST↓,
TumCP↓, UA inhibited tumorigenesis and cancer cell proliferation, modulated apoptosis and cell cycle progression and promoted autophagy
Apoptosis↑,
TumCCA↑,
TumAuto↑,
tumCV↓, UA inhibited the viability and migration of T47D, MCF-7 and MDA-MB-231 breast cancer cells by targeting phosphoinositide-3-kinase/protein kinase B (PI3K/Akt)
TumCMig↓,
Glycolysis↓, Additionally, UA affected glycolysis. The effect was accompanied by decreased levels of ATP, lactate, hexokinase 2 and pyruvate kinase. I
ATP↓,
lactateProd↓,
HK2↓, The Akt inhibition affected glycolysis and markedly decreased levels of HK2, pyruvate kinase M2, ATP and lactate.
PKA↓,
COX2↓, UA may down-regulate the expression of COX-2
mtDam↑, UA significantly enhanced proapoptotic effects and stimulated mitochondrial dysfunction by activating caspases 3, 8 and 9, and downregulated Bcl-2 expression in these cancer cells.
Casp3↑,
Casp8↑,
Casp9↑,
Akt↓, UA downregulated the Akt signaling in three breast cancer cell lines
ROS↑, Derivative 17 significantly increased the production of ROS for 24 h, while 5 and 23 did so for 48 h.
MMP↓, human breast cancer cell line MDA-MB-231, UA decreased the mitochondrial ∆Ψm,
P53↑, regulatory proteins p53 and Bax were upregulated while the antiapoptotic protein Bcl-2 was downregulated following treatment with UA.
Showing Research Papers: 1 to 21 of 21
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
ROS↓, 1, ROS↑, 8,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 2, ETC↓, 1, MMP↓, 3, mtDam↑, 2, UCP1↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACAA1↓, 1, ALAT↓, 1, cMyc↓, 1, FABP4↓, 1, Glycolysis↓, 3, HK2↓, 2, lactateProd↓, 1, PCK1↓, 1, PKM2↓, 1, PLIN1↓, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 5, Apoptosis?, 1, Apoptosis↑, 6, BAX↓, 1, Bcl-2↓, 1, Casp↑, 1, Casp3↑, 2, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 2, Fas↑, 1, FasL↑, 1, JNK↑, 1, MDM2↓, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
HCAR2↑, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 3,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, HSP70/HSPA5↓, 1, HSP90↓, 2,
Autophagy & Lysosomes(tgid=9) ⓘ
BNIP3↝, 1, TumAuto↑, 3,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 2, P53↑, 1, cl‑PARP↑, 1, PCNA↓, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 1, CDK4↓, 2, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, EMT↓, 2, ERK↓, 3, HDAC↓, 2, miR-34a↓, 1, mTOR↓, 2, NOTCH1↓, 1, PI3K↓, 3, RAS↓, 1, STAT3↓, 3, TOP2↓, 1, TumCG↓, 2, Wnt↓, 1,
Migration(tgid=13) ⓘ
AP-1↓, 1, Cartilage↑, 1, COL4↓, 1, ITGA11↓, 1, Ki-67↓, 2, KRAS↓, 1, LAMB3↑, 1, MMP2↓, 1, MMP9↓, 1, PKA↓, 1, PKCδ↓, 1, Slug↓, 1, THBS2↓, 1, TRIB3↑, 1, TumCI↓, 1, TumCMig↓, 2, TumCP↓, 2, TumMeta↓, 2, TumMeta↑, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 2, Hif1a↓, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
GLUT1↓, 1, P-gp↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↓, 1, COX2↓, 4, HCAR2↑, 1, IL17↓, 4, IL22↓, 2, IL23↓, 2, IL28↓, 1, IL6↓, 2, Imm↑, 1, Inflam↓, 3, NF-kB↓, 3, NF-kB↑, 1, RANTES↓, 1, TNF-α↓, 3,
Protein Aggregation(tgid=19) ⓘ
NLRP3↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, ChemoSen↑, 3, Dose↝, 2, eff↑, 10, RadioS↑, 2, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, BMD↑, 1, GutMicro↑, 1, IL6↓, 2, Ki-67↓, 2, KRAS↓, 1, TG/TAG↓, 1, TRIB3↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 3, chemoP↑, 1, K17↓, 1,
Infection & Microbiome(tgid=24) ⓘ
CD8+↓, 1,
Total Targets: 124
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiBio↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 5, Catalase↑, 3, DPPH↓, 1, Ferroptosis↓, 1, GPx↑, 4, GPx4↓, 1, GSH↑, 4, GSR↑, 1, HDL↓, 1, HDL↑, 1, HO-1↑, 5, HO-1↝, 1, Iron↓, 1, lipid-P↓, 5, lipid-P↑, 1, MDA↓, 4, MPO↓, 1, NQO1↑, 1, Nrf1↑, 1, NRF2↓, 1, NRF2↑, 5, ROS?, 1, ROS↓, 10, ROS↝, 1, SOD↑, 5, SOD1↑, 1, TBARS↓, 1, VitC↑, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
NCOA4↝, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 2, AMPK↓, 1, AMPK↑, 1, LDL↓, 3, NAD↓, 1, NADPH↓, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Apoptosis↓, 3, BAX↓, 1, Bcl-2↓, 1, Casp3↓, 2, Casp9↓, 2, Cyt‑c↓, 2, Ferroptosis↓, 1, GADD34↓, 1, iNOS↓, 2, JNK↓, 1, MAPK↓, 2,
Transcription & Epigenetics(tgid=7) ⓘ
other↓, 1, other↑, 2, other↝, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↓, 1, HSP70/HSPA5↓, 1, HSP70/HSPA5↑, 1, HSPs↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↓, 1, LC3II↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, P53↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, p‑ERK↓, 1, GSK‐3β↓, 4, HDAC↓, 1, mTOR↓, 1, PI3K↓, 1, STAT3↓, 2, tyrosinase↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, CDK5↓, 1, E-sel↓, 1, MMP9↓, 2, Snail↑, 1, Treg lymp↓, 1, Twist↑, 1, TXNIP↓, 1, VCAM-1↓, 1, Vim↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, ATF4↓, 1, NO↓, 4, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
GastroP↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↓, 1, CD4+↑, 2, CD69↓, 1, COX1↓, 1, COX2↓, 6, CRP↓, 1, CTLA-4↓, 1, CXCc↓, 1, CXCR4↓, 2, ICAM-1↓, 1, IFN-γ↓, 7, IKKα↓, 2, IL1↓, 1, IL10↓, 3, IL10↑, 4, IL12↓, 1, IL17↓, 17, IL18↓, 1, IL1β↓, 9, IL2↓, 2, IL22↓, 2, IL23↓, 2, IL4↓, 1, IL6↓, 10, IL8↓, 3, Imm↓, 1, Imm↑, 1, Inflam↓, 14, MCP1↓, 4, MIP‑1α↓, 1, NF-kB↓, 5, PGE2↓, 4, TLR4↓, 2, TNF-α↓, 11, TNF-α↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 3, BDNF↓, 1, BDNF↑, 1, tau↓, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 4, BACE↓, 1, NLRP3↓, 1, XO↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
GR↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 2, BioAv↑, 1, Dose?, 1, Dose⇅, 1, eff↑, 3, eff↝, 1, Half-Life↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 2, AST↓, 2, BP↓, 1, CRP↓, 1, GutMicro↑, 2, IL6↓, 10,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiDiabetic↑, 3, cardioP↑, 1, hepatoP↑, 6, memory↑, 2, neuroP↑, 7, OS↑, 1, Pain↓, 1, PDE4↓, 1, RenoP↑, 1, toxicity↓, 1, toxicity↝, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 160
Scientific Paper Hit Count for: IL17, Interleukin-17
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#:540 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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