TLR2 Cancer Research Results
TLR2, Toll-Like Receptor 2: Click to Expand ⟱
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TLR2 is a member of the Toll-like receptor (TLR) family, which plays a key role in the innate immune system by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). TLR2 is unique in its ability to form heterodimers with other TLRs (such as TLR1 and TLR6) to broaden its ligand specificity.
TLR2 is often described as having a “double-edged sword” role. On one side, stimulation of TLR2 can enhance the immune system’s ability to detect and destroy tumor cells. On the other side, persistent TLR2 signaling may lead to a pro-tumorigenic environment characterized by the secretion of growth factors, angiogenic signals, and immune suppressive cytokines that facilitate tumor progression.
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Scientific Papers found: Click to Expand⟱
AntiCan↑, Baicalin and baicalein exhibit anticancer activities against multiple cancers with extremely low toxicity to normal cells.
*toxicity↓,
BioAv↝, Baicalein permeates easily through the epithelium from the gut lumen to the blood underneath due to its low molecular mass and high lipophilicity, albeit a low presence of its transporters.
BioAv↓, In contrast, baicalin has limited permeability partly due to its larger molecular mass and higher hydrophilicity [24]. The overall low water solubility of baicalin and baicalein contributes to their poor bioavailability.
*ROS↓, baicalin protected macrophages against mycoplasma gallisepticum (MG)-induced ROS production and NLRP3 inflammasome activation by upregulating autophagy and TLR2-NFκB pathway
*TLR2↓,
*NF-kB↓,
*NRF2↑, Therefore, baicalin exerts strong antioxidant activity by activating NRF2 antioxidant program.
*antiOx↑,
*Inflam↓, These data suggest that by attenuating ROS and inflammation baicalein inhibits tumor formation and metastasis.
HDAC1↓, baicalein reduced CTCLs by inhibiting HDAC1 and HDAC8 and its effect on tumor inhibition was better than traditional HDAC inhibitors
HDAC8↓,
Wnt↓, Baicalein also reduced the proliferation of acute T-lymphoblastic leukemia (TLL) Jurkat cells by inhibiting the Wnt/β-catenin signaling pathway
β-catenin/ZEB1↓,
PD-L1↓, baicalein and baicalin promoted antitumor immune response by suppressing PD-L1 expression of HCC cells, thus increasing tumor regression
Sepsis↓, Baicalein can also attenuate severe sepsis via ameliorating immune dysfunction of T lymphocytes.
NF-kB↓, downregulation of NFκB and CD74/CD44 signaling in EBV-transformed B cells
LOX1↓, baicalein is considered to be an inhibitor of lipoxygenases (LOXs)
COX2↓, inhibits the expression of NF-κB/p65 and COX-2
VEGF↑, Baicalin was shown to suppress the expression of VEGF, resulting in the inhibition of PI3K/AKT/mTOR pathway and reduction of proliferation and migration of human mesothelioma cells
PI3K↓,
Akt↓,
mTOR↓,
MMP2↓, baicalin suppressed expression of MMP-2 and MMP-9 via restriction of p38MAPK signaling, resulting in reduced breast cancer cell growth, invasion
MMP9↓,
SIRT1↑, The inhibition of MMP-2 and MMP-9 expression in NSCLC cells is mediated by activating the SIRT1/AMPK signaling pathway.
AMPK↑,
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*BioAv↓, Nevertheless, the inherent low bioavailability of chlorogenic acid poses challenges in practical deployments.
*Inflam↓, chlorogenic acid predominantly impedes the synthesis and secretion of inflammatory mediators such as TNF-α, NO, COX-2, and PGE2.
*TNF-α↓,
*NO↓,
*COX2↓,
*PGE2↓,
*NF-kB↓, Inhibition of NF-κB signaling pathway
*IL6↓, downregulates inflammatory mediators including IL-6, TNF-α, IL-1β, and TLR2 by hindering the phosphorylation of NF-κB pathway proteins,
*IL1β↓,
*TLR2↓,
*MAPK↓, Inhibition of MAPK signaling pathway
*NRF2↓, Activation of the Nrf2 signaling pathway
*HO-1↑, concomitant upregulation of HO-1 and NQO-1
*NQO1↑,
*cardioP↑, its cardioprotective attributes are further elucidated through modulating pertinent signaling pathways
*neuroP↑, This neuroprotection appears to correlate with an upregulation in SOD2 expression facilitated by chlorogenic acid
*SOD↑,
*GSH↑, compound bolsters SOD activity, elevates GSH concentrations, curtails ROS and LDH production, reduces MDA accumulation, and ameliorates cerebral ischemia-reperfusion (CI/R) injury sequels
*ROS↓,
*LDH↓,
*MDA↓,
*cognitive↑, Chlorogenic acid ameliorates such cognitive deficits, a process conceivably attributed to its inhibitory action on NF-κB and IL-6 within frontal brain structures (
*eff↑, One pivotal investigation showcased that bovine serum albumin (BSA)-facilitated chlorogenic acid silver nanoparticles (AgNPs-CGA-BSA) exude substantial antioxidant and anti-neoplastic properties across in vivo and in vitro matrices.
*TLR2↓, inhibits TLR2 expression in CF bronchial epithelial cell line, CFBE41o- cells
*Sp1/3/4↓, Interestingly, curcumin treatment decreased nuclear expression of transcription factor specificity protein 1 (SP1),
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*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.
*Inflam↑, already known anti-inflammatory, cardiovascular protection, antiangiogenesis, antidiabetes, hypoglycemic, antioxidation, neuroprotection, gastrointestinal protection, and antibacterial activities of MG.
*cardioP↑,
*angioG↓,
*antiOx↑,
*neuroP↑,
*Bacteria↓,
AntiTum↑, Antitumor Activity
TumCG↓, MG suppressed the growth, migration, and invasion of tumor cells and promoted apoptosis
TumCMig↓,
TumCI↓,
Apoptosis↑,
E-cadherin↑, In MCF-7 cells, MG (20 μM) increased the expression of the tumor suppressor miRNA miR-200c to inhibit zinc finger E-box-binding homeobox 1 and increased the expression of E-cadherin
NF-kB↓, regulated the NF-κB pathway, induced cell cycle arrest, downregulated cyclin D1, and inhibited the expression of proliferating cell nuclear antigen (PCNA), Ki67, matrix metalloproteinase (MMP)-2, MMP-7, and MMP-9
TumCCA↑,
cycD1/CCND1↓,
PCNA↓,
Ki-67↓,
MMP2↓,
MMP7↓,
MMP9↓,
TumCG↓, A549 cells, MG (1–50 μM) showed growth inhibition and autophagy via activating caspase-3 and poly-(ADP)-ribose polymerase cleavage, reducing NF-κB/Rel A and Akt/mTOR pathway expression, dose-dependently blocking mitosis and G2/M progression, and incr
Casp3↑,
NF-kB↓,
Akt↓,
mTOR↓,
LDH↓,
Ca+2↑, MG (20–100 μM) played roles of [Ca2+] increase,
eff↑, cotreatment with MG and honokiol exerted a synergistic antitumor effect to induce cell cycle arrest as well as autophagy and inhibit proliferation by decreasing cyclin A/D1, cyclin-dependent kinase 2, 4, 6, p-PI3K, p-Akt, Ki67, p-p38, and p-JNK and
*toxicity↓, In summary, MG was found to be fairly nontoxic.
*BioAv↝, In recent years, the bioavailability of MG has been significantly improved by various formulations including solid dispersion, phospholipid complex, nanoparticles, emulsion, mixed micelles
*PGE2↓, exert neuroprotective activities by inhibiting the production of PGE2, regulating (GABA)A receptor subtypes
*TLR2↓, MG inhibited TLR2/TLR4/NF-κB/MAPK/PPAR-γ pathways and decreased the expression of inflammatory cytokines to exhibit anti-inflammatory activity.
*TLR4↓,
*MAPK↓,
*PPARγ↓,
TumCA↓, Shikonin (1 μm) inhibited significantly the adhesion, invasion and migratory ability of MGC-803 cells.
TumCI↓,
TumCMig↓,
MMP2↓, matrix metalloproteinases (MMP)-2, MMP-7, TLR2 and p65 NF-κB
MMP7↓,
TLR2↓,
p65↓,
NF-kB↓,
eff↑, In addition, the co-incubation of Shikonin and anti-TLR2/MG-132 has a significant stronger activity than anti-TLR2 or MG-132 alone.
ROS↑, Shikonin-induced ROS generation
*Inflam↓, reported by several previous studies for its potent anti-inflammatory effec
*memory↑, TQ in improving learning and memory, using a rat model of AD induced by a combination of aluminum chloride (AlCl3) and d-galactose (d-Gal).
*cognitive↑, TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses
*Aβ↓,
*TNF-α↓, Fourteen consecutive days of TQ treatment at all levels of doses caused a significant decrease in the rats brain content of TNF-α compared to AD group reaching 39.85, 18.22, and 30.37 versus 65.30, respectively
*IL1β↓, TQ at all levels of doses significantly reduced the brain content of IL-1β compared to AD group reaching 36.55, 14.32, and 27.27 versus 53.65
*TLR2↓, TQ middle dose (20 mg/kg) significantly downregulated the expression of TLR-2 by 82.74% and 77.94% and the expression of TLR-4 by 84.35% and 63.30%,
*NF-kB↓, and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses
*IRF3↓, expression of IRF-3 by 18.19% and 77.96%,
TLR4↓,
MyD88↓, expression of MyD88 by 79.65% and 68.36%
TRIF↓, expression of TRIF by 25.90% and 76.75%
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*antiOx↑, promising potential in the prevention and treatment of AD due to its significant antioxidative, anti-inflammatory,
*Inflam↓, anti-inflammatory activity of TQ is mediated through the Toll-like receptors (TLRs)
*AChE↓, In addition, it shows anticholinesterase activity and prevents α-synuclein induced synaptic damage.
AntiCan↑, NS plant, has been proven to have a wide range of pharmacological interventions, including antidiabetic, anticancer, cardioprotective, retinoprotective, renoprotective, neuroprotective, hepatoprotective and antihypertensive effects
*cardioP↑,
*RenoP↑,
*neuroP↑,
*hepatoP↑,
TumCG↓, potential ability to inhibit tumor growth by stimulating apoptosis as well as by suppression of the P13K/Akt pathways, cell cycle arrest and by inhibition of angiogenesis
Apoptosis↑,
PI3K↓,
Akt↑,
TumCCA↑,
angioG↓,
*NF-kB↓, TQ inhibits nuclear translocation of NF-kB which subsequently blocks the production of NF-kB mediated neuroinflammatory cytokines
*TLR2↓, TQ administration at different doses (10, 20, 40 mg/kg) significantly down-regulated the mRNA expression of TLR-2, TLR-4, MyD88, TRIF and their downstream effectors Interferon regulatory factor 3 (IRF-3)
*TLR4↓,
*MyD88↓,
*TRIF↓,
*IRF3↓,
*IL1β↓, TQ also inhibits LPS induced pro-inflammatory cytokine release like IL-1B, IL-6 and IL-12 p40/70 via its interaction with NF-kB
*IL6↓,
*IL12↓,
*NRF2↑, Nuclear erythroid-2 related factor/antioxidant response element (Nrf 2/ARE) being an upstream signaling pathway of NF-kB signaling pathway, its activation by TQ
*COX2↓, TQ also inhibits the expression of all genes regulated by NF-kB, i.e., COX-2, VEGF, MMP-9, c-Myc, and cyclin D1 which distinctively lowers NF-kB activation making it a potentially effective inhibitor of inflammation, proliferation and invasion
*VEGF↓,
*MMP9↓,
*cMyc↓,
*cycD1/CCND1↓,
*TumCP↓,
*TumCI↓,
*MDA↓, it prevents the rise of malondialdehyde (MDA), transforming growth factor beta (TGF-β), c-reactive protein, IL1-β, caspase-3 and concomitantly upregulates glutathione (GSH), cytochrome c oxidase, and IL-10 levels [92].
*TGF-β↓,
*CRP↓,
*Casp3↓,
*GSH↑,
*IL10↑,
*iNOS↑, decline of inducible nitric oxide synthase (iNOS) protein expression
*lipid-P↓, TQ prominently mitigated hippocampal lipid peroxidation and improved SOD activity
*SOD↑,
*H2O2↓, TQ is a strong hydrogen peroxide, hydroxyl scavenger and lipid peroxidation inhibitor
*ROS↓, TQ (0.1 and 1 μM) ensured the inhibition of free radical generation, lowering of the release of lactate dehydrogenase (LDH)
*LDH↓,
*Catalase↑, upsurge the levels of GSH, SOD, catalase (CAT) and glutathione peroxidase (GPX)
*GPx↑,
*AChE↓, TQ exhibited the highest AChEI activity of 53.7 g/mL in which NS extract overall exhibited 84.7 g/mL, which suggests a significant AChE inhibition.
*cognitive↑, Most prominently, TQ has been found to regulate neurite maintenance for cognitive benefits by phosphorylating and thereby activating the MAPK protein, particularly the JNK proteins for embryogenesis and also lower the expression levels of BAX
*MAPK↑,
*JNK↑,
*BAX↓,
*memory↑, TQ portrays its potential of spatial memory enhancement by reversing the conditions as observed by MWM task
*Aβ↓, TQ thus, has been shown to ameliorate the Aβ accumulation
*MMP↑, improving the cellular activity, inhibiting mitochondrial membrane depolarization and suppressing ROS
*Inflam↓, (TQ), the main active constituent of Nigella sativa oil, has been reported by several previous studies for its potent anti-inflammatory effect.
*Aβ↓, TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses
*TNF-α↓, TQ treatment at all levels of doses caused a significant decrease in the rats brain content of TNF-a compared to AD group reach-
ing 39.85, 18.22, and 30.37 versus 65.30, r
*IL1β↓,
*TLR2↓, and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses ( p < 0.05).
*IRF3↓,
*TLR4↓, TQ inhibits TLR-2 and TLR-4 and their downstream signaling molecule in a dose independent manner
*memory↑, TQ improves learning and memory ability in AD rat model
*NF-kB↓, TQ at all levels of doses for
14 consecutive days caused a significant decrease in
NF-B expression
*MyD88↓, TQ middle dose (20 mg/kg) significantly downregulated the expression of TLR-2 by 82.74% and 77.94% and the expression of TLR-4
by 84.35% and 63.30%, the expression of MyD88
by 79.65% and 68.36%, the expression of TRIF by
25.90% and 76.75%,
*TRIF↓,
*BBB↑, t crosses the blood
brain barrier and exerts diverse therapeutic effects
with respect to neuroinflammation.
*cognitive↑, Thus, we can hypothesize that TQ could improve cognition and the brain morphological changes by attenuating the detrimental inflammatory effect of the pro-inflammatory cytokines release
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*BioAv↓, TQ has poor bioavailability and is hydrophobic, prohibiting clinical trials with TQ alone.
*BioAv↑, TQ nanoparticle formulation shows better bioavailability than free TQ,
*Inflam↓, anti-inflammatory effects of TQ involve multiple complex signaling pathways as well as molecular mechanisms
*antiOx↑, antioxidant activity from the inhibition of oxidative stress
*ROS↓,
*GSH↑, GSH prevented ROS-mediated oxidative stress damage
*GSTs↑, TQ was found to exhibit antioxidant properties by increasing the levels of GSH and glutathione-S-transferase enzyme alpha-3 (GSTA3)
*MPO↓, TQ significantly reduced the disease activity index (DAI) and myeloperoxidase (MPO) activity, protecting the internal microenvironment of the colon.
*NF-kB↓, TQ reduced NF-κB signaling gene expression while alleviating the increase of COX-2 in skin cells induced by 12-O-tetradecanoylphorbol-13-acetate
*COX2↓,
*IL1β↓, reduced the expression of inflammatory factors such as IL-1β, TNF-α, IFN-γ, and IL-6
*TNF-α↓,
*IFN-γ↓,
*IL6↓,
*cardioP↑, TQ may exhibit substantial effects in the control of inflammation in CVD
*lipid-P↓, TQ reduces lipid accumulation and enhances antioxidant capacity and renal function.
*TAC↑,
*RenoP↑,
Apoptosis↑, Breast cancer TQ induces apoptosis and cell cycle arrest; reduces cancer cell proliferation, colony formation, and migration;
TumCCA↑,
TumCP↓,
TumCMig↓,
angioG↓, Colorectal Cancer (CRC) TQ inhibits the angiogenesis
TNF-α↓, Lung cancer TQ inhibits tumor cell proliferation by causing lung cancer cell apoptosis to significantly arrest the S phase cell cycle and significantly reduce the activity of TNF-a and NF-κB
NF-kB↓,
ROS↑, Pancreatic cancer TQ significantly increases the level of ROS production in human pancreatic cancer cells
EMT↓, TQ initiates the miR-877-5p and PD-L1 signaling pathways, inhibiting the migration and EMT of bladder cancer cells.
*Aβ↓, TQ significantly reduced the expression of Aβ, phosphorylated-tau, and BACE-1 proteins.
*p‑tau↓,
*BACE↓,
*TLR2↓, Parkinson’s disease (PD) TQ inhibits activation of the NF-κB pathway.
TQ reduces the expression of TLR-2, TLR-4, MyD88, TNF-α, IL-1β, IFN-β, IRF-3, and NF-κB.
*TLR4↓,
*MyD88↓,
*IRF3↓,
*eff↑, TQ pretreatment produced a dose-dependent reduction in the MI area and significantly reduced the elevation of serum cardiac markers caused by ISO.
eff↑, Curcumin and TQ induced apoptosis and cell cycle arrest and reduced cancer cell proliferation, colony formation, and migration in breast cancer cells
DNAdam↑, nanomedicine with TQ that induced DNA damage and apoptosis, inhibited cell proliferation, and prevented cell cycle progression
*iNOS↓, TQ significantly reduced the expression of COX-2 and inducible nitric oxide synthase (iNOS)
*Dose↝, EO, which contained 25 % thymol and 25 % carvacrol as active components. (0, 60, 120, or 240 mg/kg)
*OCLN↑, occludin gene expression tended to be up-regulated linearly with increasing EO dosages
*TLR2↓, linearly inhibited the mRNA expression of TLR2 and tumor necrotic factor-α in the ileum
*TNF-α↓,
Bacteria↓, The beneficial effects of EO on intestinal lesions and histomorphology might be associated with their antibacterial activity and stabilizing effects on intestinal microflora
GutMicro↑,
Showing Research Papers: 1 to 11 of 11
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↓, 1, ROS↑, 2,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, LDH↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 2, Akt↑, 1, Apoptosis↑, 3, Casp3↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, HDAC1↓, 1, HDAC8↓, 1, mTOR↓, 2, PI3K↓, 2, TumCG↓, 3, Wnt↓, 1,
Migration ⓘ
Ca+2↑, 1, E-cadherin↑, 1, Ki-67↓, 1, MMP2↓, 3, MMP7↓, 2, MMP9↓, 2, TumCA↓, 1, TumCI↓, 2, TumCMig↓, 3, TumCP↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, LOX1↓, 1, VEGF↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, MyD88↓, 1, NF-kB↓, 5, p65↓, 1, PD-L1↓, 1, PGE2↓, 1, TLR2↓, 1, TLR4↓, 1, TNF-α↓, 1, TRIF↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↝, 1, eff↑, 3,
Clinical Biomarkers ⓘ
GutMicro↑, 1, Ki-67↓, 1, LDH↓, 1, PD-L1↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, AntiTum↑, 1, cardioP↑, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1, Sepsis↓, 1,
Total Targets: 56
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 5, Catalase↑, 2, GPx↑, 1, GSH↑, 4, GSTs↑, 2, H2O2↓, 1, HO-1↑, 2, lipid-P↓, 3, MDA↓, 3, MPO↓, 1, NOX4↓, 1, NQO1↑, 1, NRF2↓, 1, NRF2↑, 3, ROS↓, 5, SOD↑, 3, TAC↑, 2,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, CRM↑, 1, LDH↓, 2, PPARγ↓, 1,
Cell Death ⓘ
BAX↓, 1, Casp3↓, 1, iNOS↓, 2, iNOS↑, 1, JNK↑, 1, MAPK↓, 2, MAPK↑, 1,
Kinase & Signal Transduction ⓘ
Sp1/3/4↓, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, STAT3↓, 1,
Migration ⓘ
MMP9↓, 1, TGF-β↓, 1, TumCI↓, 1, TumCP↓, 1, VCAM-1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, NO↓, 2, VEGF↓, 1,
Barriers & Transport ⓘ
BBB↑, 1, OCLN↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 3, CRP↓, 1, ICAM-1↓, 1, IFN-γ↓, 1, IL1↓, 1, IL10↑, 1, IL12↓, 1, IL1β↓, 6, IL6↓, 4, IL8↓, 1, Inflam↓, 7, Inflam↑, 1, MyD88↓, 3, NF-kB↓, 7, PGE2↓, 2, TLR2↓, 10, TLR4↓, 5, TNF-α↓, 6, TRIF↓, 2,
Synaptic & Neurotransmission ⓘ
AChE↓, 2, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 4, BACE↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 1, BioAv↝, 1, Dose↝, 1, eff↑, 2,
Clinical Biomarkers ⓘ
BP↓, 1, creat↓, 1, CRP↓, 1, IL6↓, 4, LDH↓, 2,
Functional Outcomes ⓘ
cardioP↑, 4, cognitive↑, 4, hepatoP↑, 1, memory↑, 3, neuroP↑, 4, RenoP↑, 3, toxicity↓, 2,
Infection & Microbiome ⓘ
Bacteria↓, 1, IRF3↓, 4,
Total Targets: 85
Scientific Paper Hit Count for: TLR2, Toll-Like Receptor 2
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#:1042 State#:% Dir#:1
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