E-sel Cancer Research Results
E-sel, E-selectin: Click to Expand ⟱
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E-selectin is a cell adhesion molecule that plays a crucial role in the recruitment of leukocytes to sites of inflammation. In cancer, E-selectin is involved in the interaction between tumor cells and the endothelium, promoting metastasis and tumor progression.
E-selectin is expressed on the surface of endothelial cells in tumors, and its expression is associated with increased metastasis and poor prognosis.
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Scientific Papers found: Click to Expand⟱
*TNF-α↓, LA also strongly inhibited TNF-alpha-induced mRNA expression of monocyte chemoattractant protein-1
*NF-kB↓, LA dose-dependently inhibited TNF-alpha-induced IkappaB kinase activation, subsequent degradation of IkappaB, the cytoplasmic NF-kappaB inhibitor, and nuclear translocation of NF-kappaB.
*antiOx↑, LA in its free, non-protein-bound form has potent antioxidant and metal-chelating properties
*IronCh↑,
*GSSG↓, DHLA/LA couple may chemically reduce glutathione disulfide (GSSG) to GSH
*VCAM-1↓, E-selectin, VCAM-1, ICAM-1, and MCP-1 message levels decreased by 93%, 77%, 67%, and 100%, respectively, when HAEC were pretreated with 0.5mmol/l LA
*E-sel↓,
*ICAM-1↓,
*MCP1↓,
*NF-kB↓, Lipoic acid inhibits TNF-a-induced activation of NF-kB and degradation of IkBs
IKKα↓,
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).
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vitro+vivo, |
Nor, |
HUVECs |
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*NF-kB↓,
*p65↓, p65 was slightly decreased
*TLR4∅, protein levels of the LPS receptor Toll-like receptor 4 remained unimpaired.
*angioG↓,
*TumCP↓,
*VEGF↓,
*Inflam↓,
*ICAM-1↓,
*VCAM-1↓,
*E-sel↓,
*p‑JNK↓,
*HO-1↑,
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Review, |
AD, |
NA |
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Review, |
Stroke, |
NA |
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*Inflam↓, remarkable anti-inflammatory and antioxidant effects.
*antiOx↑,
*BioAv↑, high bioavailability and low toxicity in many species has contributed to its promising research prospects.
*toxicity↓,
*NADPH↓, Pterostilbene significantly down-regulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX),
*ROS↓, which is the key enzyme family that induces the release of reactive oxygen species (ROS)
*Catalase↑, pterostilbene treatment as it increases the expression levels of catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and other antioxidants in diabetic rats [
*GSH↑,
*SOD↑,
*TNF-α↓, (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-4), matrix metalloproteinases (MMPs), and cyclooxygenase (COX)-2 are all suppressed by pterostilbene treatment.
*IL1β↓,
*IL4↓,
*MMPs↓,
*COX2↓,
*MAPK↝, anti-inflammatory action of pterostilbene has been proved to be associated with modulating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways
*NF-kB↓,
*IL8↓, pterostilbene can successfully reverse the elevation of related pro-inflammatory cytokines (IL-8, monocyte chemoattractant protein (MCP)-1, and E-selectin)
*MCP1↓,
*E-sel↓,
*lipid-P↓, Pterostilbene has been demonstrated to reduce lipid peroxidation by regulating the expression of Nrf2, exhibiting anti-peroxidation and anti-hyperlipidemic effects
*NRF2↑,
*PPARα↑, Pterostilbene acts as a potent PPAR-α agonist
*LDL↓, pterostilbene could effectively reduce the plasma low-density lipoprotein (LDL) cholesterol levels of hamsters by 29% and increase the plasma high-density lipoprotein (HDL) cholesterol levels by almost 7%
other↓, Ability to Protect against Stroke
*Dose↝, When the shikonin concentration was >0.1 μmol/L, the cell viability increased significantly.
*Apoptosis↓, SKN Reduces ox-LDL-Induced Endothelial Cell Apoptosis
*Casp3↓, SKN pretreatment downregulated the cleaved caspase-3 protein levels and upregulated Bcl-2 protein levels in a concentration-dependent manner.
*Bcl-2↑,
*Inflam↓, SKN Downregulates the Expression of Inflammatory Factors Induced by ox-LDL
*VCAM-1↓, SKN pretreatment significantly downregulates the levels of VCAM1, ICAM1, and E-selectin proteins.
*ICAM-1↓,
*E-sel↓,
*ROS↓, SKN pretreatment significantly decreases the generation of ROS and increases the SOD activity induced by ox-LDL.
*SOD↑,
*AMPK↑, SKN Inhibits Oxidative Stress Damage by Activating the AMPK-Nrf2-HO-1 Pathway
*NRF2↑,
*HO-1↑,
*TNF-α↓, TNF-α, IL-1β, IL-6, VCAM1, ICAM1, and E-selectin in endothelial cells, while SKN treatment significantly downregulated the expression of these proteins mentioned above
*IL1β↓,
*IL6↓,
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
Transcription & Epigenetics ⓘ
other↓, 1,
Immune & Inflammatory Signaling ⓘ
IKKα↓, 1, Inflam↓, 1,
Total Targets: 3
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↑, 1, GSR↑, 1, GSSG↓, 1, HO-1↑, 3, lipid-P↓, 1, MDA↓, 1, NRF2↑, 2, ROS↓, 2, SOD↑, 3,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, LDL↓, 1, NADPH↓, 1, PPARα↑, 1,
Cell Death ⓘ
Apoptosis↓, 1, Bcl-2↑, 1, Casp3↓, 1, p‑JNK↓, 1, MAPK↓, 1, MAPK↝, 1,
Migration ⓘ
E-sel↓, 5, MMPs↓, 1, TumCP↓, 1, VCAM-1↓, 4,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, NO↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, ICAM-1↓, 4, IFN-γ↓, 1, IKKα↓, 1, IL10↑, 2, IL12↓, 1, IL17↓, 1, IL1β↓, 3, IL2↓, 1, IL4↓, 1, IL6↓, 2, IL8↓, 2, Inflam↓, 3, MCP1↓, 2, NF-kB↓, 5, p65↓, 1, PGE2↓, 1, TLR4∅, 1, TNF-α↓, 3, TNF-α↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, Dose↝, 1,
Clinical Biomarkers ⓘ
IL6↓, 2,
Functional Outcomes ⓘ
toxicity↓, 1,
Total Targets: 54
Scientific Paper Hit Count for: E-sel, E-selectin
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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