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首页> 外文期刊>Archives of pharmacal research >Apoptotic effect of propyl gallate in activated rat hepatic stellate cells.
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Apoptotic effect of propyl gallate in activated rat hepatic stellate cells.

机译:没食子酸丙酯在活化的大鼠肝星状细胞中的凋亡作用。

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摘要

Hepatic stellate cells (HSCs) play a central role in liver fibrosis. Inhibition of HSC growth and induction of apoptosis have been proposed as therapeutic strategies for the treatment and prevention of liver fibrosis. Propyl gallate (PG) is an antioxidant widely used in processed foods, cosmetics and medicinal preparations. However, the anti-fibrotic effect of PG in liver injury is unclear. In this study, we investigated whether PG could induce apoptosis in activated HSCs. Treatment of activated HSCs with PG inhibited cell viability in a dose- and time-dependent manner. PG induced apoptosis as demonstrated by morphological changes, poly(ADP-ribose) polymerase (PARP) cleavage, caspase-3 cleavage, increased Bad expression, and decreased Bcl-2 protein expression. Through stimulation of the activation of c-Jun NH2-terminal protein kinase (JNK) and p38 mitogen-activated protein kinases (MAPK) by PG treatment, we demonstrated that JNK and p38 MPAK are not involved in PG-induced apoptosis using their specific inhibitors. Taken together, these findings indicate that PG induces apoptosis in activated HSCs. The potential anti-fibrotic effect of PG warrants further evaluation.
机译:肝星状细胞(HSC)在肝纤维化中起重要作用。已经提出抑制HSC生长和诱导凋亡是治疗和预防肝纤维化的治疗策略。没食子酸丙酯(PG)是一种抗氧化剂,广泛用于加工食品,化妆品和药物制剂中。但是,PG在肝损伤中的抗纤维化作用尚不清楚。在这项研究中,我们调查了PG是否可以在活化的HSCs中诱导凋亡。用PG处理活化的HSCs以剂量和时间依赖性方式抑制细胞活力。 PG诱导凋亡,如形态学改变,聚(ADP-核糖)聚合酶(PARP)裂解,caspase-3裂解,Bad表达增加和Bcl-2蛋白表达减少所证明。通过PG处理刺激c-Jun NH2末端蛋白激酶(JNK)和p38丝裂原活化蛋白激酶(MAPK)的激活,我们证明了JNK和p38 MPAK使用它们的特异性抑制剂不参与PG诱导的细胞凋亡。 。综上所述,这些发现表明PG诱导了活化的HSC中的细胞凋亡。 PG的潜在抗纤维化作用值得进一步评估。

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