IL18 Cancer Research Results
IL18, Interleukin 18: Click to Expand ⟱
| Source: |
| Type: |
High levels of IL-18 production may play a major role in the growth and metastasis of renal cancer. Higher expression of IL-18 is detected in various cancer cells.
IL-18 is often expressed in various cancers, including melanoma, colorectal cancer, breast cancer, and gastric cancer. Its expression can vary depending on the tumor type and the immune context.
Elevated levels of IL-18 are frequently associated with the presence of tumor-infiltrating immune cells and can be produced by both immune and tumor cells.
High levels of IL-18 expression are often associated with a favorable prognosis in various cancers. Elevated IL-18 levels in the tumor microenvironment can correlate with increased immune cell infiltration and better overall survival.
|
Scientific Papers found: Click to Expand⟱
*p‑PPARγ↓, preventing the phosphorylation of peroxisome proliferator-activated receptors (PPARγ)
*cardioP↑, cardioprotective activity by AMP-activated protein kinase (AMPK) activation and suppressing mitochondrial apoptosis.
*AMPK↑,
*BioAv↝, The oral bioavailability was found to be 32.4 ± 4.8% after 5 mg/kg intravenous and 10 mg/kg oral WA administration.
*Half-Life↝, The stability studies of WA in gastric fluid, liver microsomes, and intestinal microflora solution showed similar results in male rats and humans with a half-life of 5.6 min.
*Half-Life↝, WA reduced quickly, and 27.1% left within 1 h
*Dose↑, WA showed that formulation at dose 4800 mg having equivalent to 216 mg of WA, was tolerated well without showing any dose-limiting toxicity.
*chemoPv↑, Here, we discuss the chemo-preventive effects of WA on multiple organs.
IL6↓, attenuates IL-6 in inducible (MCF-7 and MDA-MB-231)
STAT3↓, WA displayed downregulation of STAT3 transcriptional activity
ROS↓, associated with reactive oxygen species (ROS) generation, resulted in apoptosis of cells. The WA treatment decreases the oxidative phosphorylation
OXPHOS↓,
PCNA↓, uppresses human breast cells’ proliferation by decreasing the proliferating cell nuclear antigen (PCNA) expression
LDH↓, WA treatment decreases the lactate dehydrogenase (LDH) expression, increases AMP protein kinase activation, and reduces adenosine triphosphate
AMPK↑,
TumCCA↑, (SKOV3 andCaOV3), WA arrest the G2/M phase cell cycle
NOTCH3↓, It downregulated the Notch-3/Akt/Bcl-2 signaling mediated cell survival, thereby causing caspase-3 stimulation, which induces apoptosis.
Akt↓,
Bcl-2↓,
Casp3↑,
Apoptosis↑,
eff↑, Withaferin-A, combined with doxorubicin, and cisplatin at suboptimal dose generates ROS and causes cell death
NF-kB↓, reduces the cytosolic and nuclear levels of NF-κB-related phospho-p65 cytokines in xenografted tumors
CSCs↓, WA can be used as a pharmaceutical agent that effectively kills cancer stem cells (CSCs).
HSP90↓, WA inhibit Hsp90 chaperone activity, disrupting Hsp90 client proteins, thus showing antiproliferative effects
PI3K↓, WA inhibited PI3K/AKT pathway.
FOXO3↑, Par-4 and FOXO3A proapoptotic proteins were increased in Pten-KO mice supplemented with WA.
β-catenin/ZEB1↓, decreased pAKT expression and the β-catenin and N-cadherin epithelial-to-mesenchymal transition markers in WA-treated tumors control
N-cadherin↓,
EMT↓,
FASN↓, WA intraperitoneal administration (0.1 mg) resulted in significant suppression of circulatory free fatty acid and fatty acid synthase expression, ATP citrate lyase,
ACLY↓,
ROS↑, WA generates ROS followed by the activation of Nrf2, HO-1, NQO1 pathways, and upregulating the expression of the c-Jun-N-terminal kinase (JNK)
NRF2↑,
HO-1↑,
NQO1↑,
JNK↑,
mTOR↓, suppressing the mTOR/STAT3 pathway
neuroP↑, neuroprotective ability of WA (50 mg/kg b.w)
*TNF-α↓, WA attenuate the levels of neuroinflammatory mediators (TNF-α, IL-1β, and IL-6)
*IL1β↓,
*IL6↓,
*IL8↓, WA decreases the pro-inflammatory cytokines (IL-6, TNFα, IL-8, IL-18)
*IL18↓,
RadioS↑, radiosensitizing combination effect of WA and hyperthermia (HT) or radiotherapy (RT)
eff↑, WA and cisplatin at suboptimal dose generates ROS and causes cell death [41]. The actions of this combination is attributed by eradicating cells, revealing markers of cancer stem cells like CD34, CD44, Oct4, CD24, and CD117
| - |
in-vitro, |
GBM, |
U251 |
|
|
|
- |
in-vitro, |
GBM, |
U87MG |
|
|
|
Casp1↓, berberine significantly inhibits inflammatory cytokine Caspase-1 activation via ERK1/2 signaling and subsequent production of IL-1β and IL-18 by glioma cells.
ERK↓, berberine induces senescence of human glioma cells by downregulating the extracellular kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway
IL1β↓, Berberine Exhibit Inhibitory Effects on Caspase-1, IL-18, and IL-1β Proteins
IL18↓,
EMT↑, berberine can reverse the process of epithelial-mesenchymal transition. aken together, these results suggest that berberine can inhibit the process of EMT
*IL1β↓, capsaicin ameliorated LPS-induced cytotoxicity in vitro and attenuated the release of interleukin (IL)-1β and IL-18.
*IL18↓,
*TRPV1↑, Molecularly, capsaicin activated transient receptor potential cation channel subfamily V member 1 –mitochondrial uncoupling protein 2 axis and inhibited caspase-1-mediated pyroptosis
*ROS↓, capsaicin alleviated LPS-induced ROS production and mitochondrial membrane potential disruption and inhibited apoptosis.
*MMP↑,
*Apoptosis↓,
*RenoP↑, These findings suggest that capsaicin shows a protective effect in in vitro acute kidney injury model.
*Inflam↓, Capsaicin ameliorates LPS-induced cytotoxicity and inflammation response in HK-2 cells
*UCPs↑, Capsaicin alleviates LPS-induced pyroptosis in HK-2 cells by activating TRPV1/UCP2 axis
| - |
Review, |
Arthritis, |
NA |
|
|
|
- |
Review, |
IBD, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
*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;
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,
| - |
in-vitro, |
Nor, |
NA |
|
|
|
- |
in-vivo, |
Nor, |
NA |
|
|
|
*RenoP↑, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage.
*NLRP3↓, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including TXNIP, ASC, caspase‐1, and IL‐1β, as well as the levels of ROS and inflammatory factors such as TNF‐α, IL‐6, and IL‐18.
*TXNIP↓,
*ASC↓,
*Casp1↓,
*IL1β↓,
*ROS↓,
*TNF-α↓,
*IL6↓,
*IL18↓,
TumCMig↓, luteolin inhibited migration and colony formation in HeLa cells.
DNMTs↓, Luteolin decreased DNMT activity in HeLa cells in a concentration-dependent manner.
HDAC↓, Luteolin Decreases HDAC Activity in HeLa Cells
HATs↓, Luteolin Reduces the HAT Activity in a Dose-Dependent Manner
ac‑H3↓, H3 acetylation marks were diminished after treatment with the 20 µM of luteolin
ac‑H4↓, the acetylation marks at H4 were also modulated,
MMP2↓, Luteolin resulted in downregulation of expression of various proteins related to migration and inflammation in HeLa cells, and fold changes (FC) after treatment with 10 and 20 µM for 48 h are given, respectively, for MMP2 (FC 0.33, 0.26), MMP3 (FC 0.
MMP9↓,
HO-1↓, Genes related to cell proliferation, growth, and apoptosis such as BCL-X (FC 0.55, 0.45), HO-1/HMOX1 (FC 0.40, 0.25), Kallikrein6 (FC 0.55, 0.48), Kallikrein 3/PSA (FC 0.58, 0.48) were reduced.
E-cadherin↑, E-cadherin (FC 1.8, 2.9) were upregulated
EZH2↓, Luteolin has depicted increased expression of MiR-26a, which is a regulator of EZH2, and at the same time, it has inhibited EZH2
HER2/EBBR2↓, luteolin treatment decreased the inflammatory and migratory proteins such as MMp-2, MMP-3, HO-1/HMOX1, Her1, HER2, Her4, mesothelin, cathepsin B, MUC1, nectin 4, FOXC2, IL-18 BPa, CCL3/MIP-1α, CXCL8/IL-8, IL-2
IL18↓,
IL8↓,
IL2↓,
*hepatoP↑, Due to its excellent liver protective effect, luteolin is an attractive molecule for the development of highly promising liver protective drugs.
*AMPK↑, fig2
*SIRT1↑,
*ROS↓,
STAT3↓,
TNF-α↓,
NF-kB↓,
*IL2↓,
*IFN-γ↓,
*GSH↑,
*SREBP1↓,
*ZO-1↑,
*TLR4↓,
BAX↑, anti cancer
Bcl-2↓,
XIAP↓,
Fas↑,
Casp8↑,
Beclin-1↑,
*TXNIP↓, luteolin inhibited TXNIP, caspase-1, interleukin-1β (IL-1β) and IL-18 to prevent the activation of NLRP3 inflammasome, thereby alleviating liver injury.
*Casp1↓,
*IL1β↓,
*IL18↓,
*NLRP3↓,
*MDA↓, inhibiting oxidative stress and regulating the level of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH)
*SOD↑,
*NRF2↑, luteolin promoted the activation of the Nrf2/ antioxidant response element (ARE) pathway and NF-κB cell apoptosis pathway, thereby reversing the decrease in Nrf2 levels(lead induced liver injury)
*ER Stress↓, down regulate the formation of nitrotyrosine (NT) and endoplasmic reticulum (ER) stress induced by acetaminophen, and alleviate liver injury
*ALAT↓, ↓ALT, AST, MDA, iNOS, NLRP3 ↑GSH, SOD, Nrf2
*AST↓,
*iNOS↓,
*IL6↓, ↓TXNIP, NLRP3, TNF-α, IL-6 ↑HO-1, NQO1
*HO-1↑,
*NQO1↑,
*PPARα↑, ↓TNF-α, IL-6 IL-1β, Bax ↑PPARα
*ATF4↓, ↓ALT, AST, TNF-α, IL-6, MDA, ATF-4, CHOP ↑GSH, SOD
*CHOP↓,
*Inflam↓, Luteolin ameliorates MAFLD through anti-inflammatory and antioxidant effects
*antiOx↑,
*GutMicro↑, luteolin could significantly enrich more than 10% of intestinal bacterial species, thereby increasing the abundance of ZO-1, down regulating intestinal permeability and plasma lipopolysaccharide
| - |
in-vitro, |
GBM, |
LN229 |
|
|
|
- |
in-vitro, |
GBM, |
U87MG |
|
|
|
tumCV↓, RSV significantly inhibited cell viability in GBM cell lines LN-229 and U87-MG.
TumCP↓, it inhibited the proliferation and invasive migration ability of GBM cells, while promoting apoptosis.
TumCMig↓,
Apoptosis↑,
NLRP3↓, RSV inhibited the over-activation of the inflammasome NLRP3 through the JAK2/STAT3 signaling pathway.
JAK2↓, by inhibiting the activation of the JAK2/STAT3 signaling pathway.
STAT3↓,
IL1β↓, RSV indeed decreased the levels of inflammasome NLRP3 and its downstream IL-1β, IL-18, IL-6, and TNFα.
IL18↓,
IL6↓,
TNF-α↓,
Inflam↓, partly mediated by improving the inflammatory state of GBM
*IL18↓, SFN administration either fully or partially reversed these changes, thus restoring IL-18 and IL-1β, substantially inhibiting NLRP3 activation, and decreasing inflammation.
*IL1β↓,
*NLRP3↓,
*Inflam↓,
PKM2↓, Shikonin is a potent PKM2 inhibitor in cancer cells and macrophages
*PKM2↓,
*IL1β↓, Shikonin dose-dependently inhibited IL-1β, IL-18 and HMGB1 release in activated BMDMs following treatment with NLRP3 inflammasome activator (for example, ATP) or AIM2 inflammasome activator
*IL18↓,
*HMGB1↓,
*Casp1↓, shikonin significantly inhibited caspase-1 activation triggered by stimulation with ATP
*NLRP3↓, pharmacologic inhibition of PKM2 by shikonin selectively suppresses NLRP3 and AIM2 inflammasome activation.
*AIM2↓,
*p‑eIF2α↓, Shikonin inhibited EIF2AK2 phosphorylation (Fig. 6a) and caspase-1 activity (Fig. 6b) in PMs obtained from mice subjected to lethal endotoxemia or polymicrobial sepsis.
*Sepsis↓,
| - |
in-vitro, |
Nor, |
HUVECs |
|
|
|
- |
in-vitro, |
NA, |
NA |
|
|
|
*NF-kB↓, TQ improves perforator flap survival by inhibiting the NF-κB/NLRP3 pathway and promoting angiogenesis.
*NLRP3↓,
*angioG↑,
*MMP9↑, TQ treatment increased the levels of Cadherin-5, MMP9, and VEGF
*VEGF↑,
*OS↑, TQ enhances the survival rate and angiogenesis of multi-regional perforator flaps.
*Pyro?, TQ inhibits pyroptosis after ischemia-reperfusion injury in rat perforator flaps
*ROS↓, TQ ameliorates oxidative stress and apoptosis following ischemia-reperfusion injury in rat perforator flaps
*Apoptosis↓,
*SIRT1↑, Western blot analysis revealed that SIRT1 protein expression increased after TQ treatment,
*SOD1↑, TQ treatment increased the protein expression levels of SOD1, HO1, and eNOS in rat perforator flap tissues, t
*HO-1↑,
*eNOS↑,
*ASC?, In our current experiments, we found that TQ reduced the expression of NLRP3, GSDMD-N, Caspase-1, IL-1β, IL-18, and ASC proteins both in vivo and in vitro.
*Casp1↓,
*IL1β↓,
*IL18↓,
| - |
in-vitro, |
Melanoma, |
A375 |
|
|
|
- |
in-vivo, |
NA, |
NA |
|
|
|
TumMeta↓, Thymoquinone causes inhibition of metastasis in vivo
TumCMig↓, Thymoquinone causes inhibition of migration by activation of NLRP3 inflammasome.
NLRP3↓,
Casp1↓, Inactivation of caspase-1 by thymoquinone resulted in inhibition of IL-1β and IL-18.
IL1β↓,
IL18↓,
ROS↓, Furthermore, inhibition of reactive oxygen species (ROS) by thymoquinone resulted in partial inactivation of NLRP3 inflammasome.
NF-kB↓, as well as inhibition of NF-κB, and hence suppressing growth and migration of melanoma cells.
Showing Research Papers: 1 to 13 of 13
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
HO-1↓, 1, HO-1↑, 1, NQO1↑, 1, NRF2↑, 2, OXPHOS↓, 1, ROS↓, 2, ROS↑, 2,
Mitochondria & Bioenergetics ⓘ
ETC↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 1, AMPK↑, 1, FASN↓, 1, IR↓, 1, LDH↓, 1, PKM2↓, 1, PPARγ↑, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 3, BAX↑, 1, Bcl-2↓, 2, Casp1↓, 2, Casp3↑, 1, Casp8↑, 1, DR5↑, 1, Fas↑, 3, FasL↑, 1, JNK↑, 3, MAPK↓, 1,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 2, PAK↓, 1,
Transcription & Epigenetics ⓘ
EZH2↓, 1, ac‑H3↓, 1, ac‑H4↓, 1, HATs↓, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
HSP90↓, 2,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, BNIP3↝, 1, TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNMTs↓, 1, P53↑, 1, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, EMT↓, 1, EMT↑, 1, ERK↓, 1, FGF↓, 1, FOXO3↑, 1, HDAC↓, 1, mTOR↓, 1, NOTCH1↓, 1, NOTCH3↓, 1, PI3K↓, 1, STAT1↓, 1, STAT3↓, 4, STAT4↓, 1, STAT5↓, 1,
Migration ⓘ
ATPase↓, 1, E-cadherin↑, 1, MMP2↓, 1, MMP9↓, 1, MMPs↓, 1, N-cadherin↓, 1, PDGF↓, 1, TGF-β↓, 1, TumCMig↓, 3, TumCP↓, 1, TumMeta↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EGFR↓, 1, Hif1a↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1↓, 1, IL12↓, 1, IL18↓, 5, IL1β↓, 3, IL2↓, 2, IL5↓, 1, IL6↓, 3, IL8↓, 2, Inflam↓, 1, JAK↓, 1, JAK2↓, 1, NF-kB↓, 4, TNF-α↓, 2,
Protein Aggregation ⓘ
NLRP3↓, 2,
Hormonal & Nuclear Receptors ⓘ
ER(estro)↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, Dose↝, 1, eff↑, 2, RadioS↑, 2,
Clinical Biomarkers ⓘ
EGFR↓, 1, EZH2↓, 1, HER2/EBBR2↓, 2, IL6↓, 3, LDH↓, 1,
Functional Outcomes ⓘ
neuroP↑, 1,
Total Targets: 100
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GSH↑, 1, HO-1↑, 2, MDA↓, 1, NQO1↑, 1, NRF2↑, 1, ROS↓, 5, SOD↑, 1, SOD1↑, 1, UCPs↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 2,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, AMPK↑, 2, PKM2↓, 1, PPARα↑, 1, p‑PPARγ↓, 1, SIRT1↑, 2, SREBP1↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↓, 2, Casp1↓, 4, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, iNOS↓, 1, MAPK↓, 1, Pyro?, 1, TRPV1↑, 1,
Transcription & Epigenetics ⓘ
other↑, 2, other↝, 2,
Protein Folding & ER Stress ⓘ
CHOP↓, 1, p‑eIF2α↓, 1, ER Stress↓, 1, HSP70/HSPA5↑, 1, HSPs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1,
Migration ⓘ
MMP9↓, 1, MMP9↑, 1, TXNIP↓, 2, ZO-1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, ATF4↓, 1, eNOS↑, 1, VEGF↑, 1,
Immune & Inflammatory Signaling ⓘ
AIM2↓, 1, ASC?, 1, ASC↓, 1, COX1↓, 1, COX2↓, 1, CRP↓, 1, CXCR4↓, 1, HMGB1↓, 1, IFN-γ↓, 1, IL17↓, 1, IL18↓, 8, IL1β↓, 8, IL2↓, 1, IL6↓, 4, IL8↓, 1, Inflam↓, 3, NF-kB↓, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 3,
Protein Aggregation ⓘ
NLRP3↓, 5,
Drug Metabolism & Resistance ⓘ
BioAv↝, 1, Dose↑, 1, Dose⇅, 1, eff↝, 1, Half-Life↝, 2,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 4,
Functional Outcomes ⓘ
cardioP↑, 1, chemoPv↑, 1, hepatoP↑, 1, neuroP↑, 1, OS↑, 1, RenoP↑, 2,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 82
Scientific Paper Hit Count for: IL18, Interleukin 18
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#:369 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page