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           Search results for: Mouse Glycogen [starch] synthase, liver(GYS2) ELISA kit SpeciesMouse   

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#27573179   2016/09/16 Save this To Up

Anticancer effect of 20(S)-ginsenoside Rh2 on HepG2 liver carcinoma cells: Activating GSK-3β and degrading β-catenin.

20(S)-ginsenoside Rh2 [(S)Rh2] possesses potential to prevent cancer in vitro as well as in vivo, but the underlying mechanism is still unknown. First, we infected HepG2 cells with lentivirus which carries β‑catenin. We detected the pharmacological effects of (S)Rh2 on HepG2 and HepG2‑β‑catenin cells and found that the IC50 of (S)Rh2 exposure on HepG2-β-catenin cells was higher than HepG2 cells. Flow cytometry (FCM) indicated that (S)Rh2 could be arrested in G0/G1 phase and induce early apoptosis in HepG2 and HepG2‑β‑catenin cells. Second, ELISA kit was used to check the activity of glycogen synthase kinase‑3β (GSK‑3β), which was upregulated by (S)Rh2. GSK‑3β inhibitor BIO, was used to verify that (S)Rh2 activated GSK‑3β. PCR and western blotting results indicated that (S)Rh2 could degrade the expression of β‑catenin, which combined with TCF in the nucleus and activate transcription of Wnt target genes, such as Bax, Bcl‑2, cyclin D1, MMP3, which were checked by chromatin immunoprecipitation (ChIP), PCR and western blotting. The results showed that the expression of Bax mRNA and proteins increased, while the cyclin D1, Bcl‑2, MMP3 mRNA and proteins were downregulated in HepG2 and HepG2‑β‑catenin cells which was induced by (S)Rh2. By contrast, with the HepG2-β-catenin + (S)Rh2 group, the expression of other mRNA and proteins in HepG2 + (S)Rh2 group changed significantly. In vivo, experiments were performed using a nude mouse xenograft model to investigate the (S)Rh2 effect. So these results suggested that (S)Rh2 could suppress proliferation, promote apoptosis and inhibit metastasis of HepG2, decrease weight of tumor by downregulating β‑catenin through activating GSK‑3β and the pharmacological effect of (S)Rh2 on HepG2 cells might be weakened by overexpression of β‑catenin.

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#24356466   2014/01/14 Save this To Up

GSK-3β inhibition attenuates LPS-induced death but aggravates radiation-induced death via down-regulation of IL-6.

Exposure of high dose ionizing radiation is lethal. Signal pathways involved in radiation biology reaction still remain illdefined. Lipopolysaccharides (LPS), the ligands of Toll-like receptor 4(TLR4), could elicit strong immune responses. Glycogen synthase kinase-3β(GSK-3β) promotes the production of inflammatory molecules and cell migration. Inhibition of GSK-3β provides protection against inflammation in animal models. The aim of the study was to investigate role of GSK-3β in LPS shock and ionizing radiation.

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#22614766   2012/06/19 Save this To Up

Wnt3a upregulates prostaglandin F2α-stimulated vascular endothelial growth factor synthesis in osteoblasts.

It is known that Wnt3a affects bone metabolism via the canonical Wnt/β-catenin signaling pathway. We have previously shown that prostaglandin F2α (PGF2α) stimulates the synthesis of vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6) via mitogen-activated protein (MAP) kinases, including p44/p42 MAP kinase, p38 MAP kinase and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the effects of Wnt3a on the synthesis of VEGF or IL-6 stimulated by PGF2α in MC3T3-E1 cells using an ELISA kit and various antibodies. Cells were cultured and pretreated with various doses of Wnt3a or SB216763, an inhibitor of glycogen synthase kinase 3β, prior to western blotting. Wnt3a significantly enhanced the PGF2α-stimulated VEGF release but had little effect on the PGF2α-stimulated IL-6 release. SB216763 markedly amplified the PGF2α-stimulated VEGF release without affecting the IL-6 release, similar to Wnt3a. Wnt3a failed to affect the PGF2α-induced phosphorylation of p44/p42 MAP kinase, p38 MAP kinase or SAPK/JNK. These results strongly suggest that Wnt3a upregulates VEGF synthesis stimulated by PGF2α via activation of the canonical pathway in osteoblasts without affecting IL-6 synthesis.

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