Chelerythrine盐酸白屈菜红碱,3895-92-9

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Chelerythrine chloride

CAS No. : 3895-92-9

MCE 国际站：Chelerythrine chloride

产品活性：Chelerythrine chloride 是一种有效，可渗透细胞的蛋白酶 C (protein kinase C) 抑制剂，能够抑制 PKC 活性，IC₅₀ 值为 660 nM。Chelerythrine chloride 抑制 Bcl-XL-Bak BH3 肽结合，IC₅₀ 为 1.5 μM，并从 Bcl-XL 取代了 Bax。Chelerythrine chloride 诱导细胞凋亡 (apoptosis) 和自噬 (autophagy)。

研究领域：Epigenetics  |  TGF-beta/Smad  |  Apoptosis  |  Autophagy

作用靶点：PKC  |  Bcl-2 Family  |  Apoptosis  |  Autophagy

In Vitro: Chelerythrine inhibits the BclXL-Bak BH3 peptide binding with IC₅₀ of 1.5 μM and displaces Bax, a BH3-containing protein, from BclXL. Mammalian cells treated with Chelerythrine undergoes apoptosis with characteristic features that suggest involvement of the mitochondrial pathway. Chelerythrine treatment inhibits LPS-induced TNF-α level and NO production in LPS-induced murine peritoneal macrophages through selective inhibition of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) activation. Moreover, the effects of chelerythrine on NO and cytokine TNF-α production can possibly be explained by the role of p38 MAPK and ERK1/2 in the regulation of inflammatory mediators expression. Chelerythrine shows cytotoxic effect on the human monocytic leukaemia cells with LD₅₀ value of 3.46 μM. Two hours after LPS stimulation, cells influenced by sanguinarine and Chelerythrine significantly decline the CCL-2 expression by a factors of 3.5 and 1.9. Chelerythrine chloride significantly enhances the phosphorylation of ERK1/2 in a dose-dependent manner. In addition, chelerythrine chloride inhibits the phosphorylation of p38.

In Vivo: Chelerythrine displays significant anti-inflammatory?effects in experimentally induced?mice?endotoxic?shock?model in vivo through inhibition of LPS-induced tumor necrosis factor-alpha (TNF-α) level and nitric oxide (NO) production in serum. Chelerythrine chloride (5 mg/kg/day, i.p.) induces apoptosis of RCC cells without significant toxicity to mice. Chelerythrine Chloride treatment leads to a dose-dependent accumulation of p53.

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