首页> 外文期刊>The Journal of Nutritional Biochemistry >Curcumin protects against thioacetamide-induced hepatic fibrosis by attenuating the inflammatory response and inducing apoptosis of damaged hepatocytes.
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Curcumin protects against thioacetamide-induced hepatic fibrosis by attenuating the inflammatory response and inducing apoptosis of damaged hepatocytes.

机译:姜黄素可通过减轻炎症反应并诱导受损肝细胞的凋亡来预防硫代乙酰胺诱导的肝纤维化。

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摘要

Inflammation and hepatic stellate cell (HSC) activation are the most crucial steps in the formation of hepatic fibrosis. Hepatocytes damaged by viral or bacterial infection, alcohol or toxic chemicals initiate an inflammatory response that activates collagen production by HSCs. Recent studies indicate curcumin has liver-protective effects due to its anti-inflammatory, antioxidant and anticancer activities; however, the mechanisms are not well understood. In this study, we show that curcumin protected against hepatic fibrosis in BALB/c mice in vivo by inhibiting HSC activation, inflammatory responses and inducing apoptosis of damaged hepatocytes. Using the thioacetamide (TAA)-induced hepatic fibrosis animal model, we found that curcumin treatment up-regulated P53 protein expression and Bax messenger RNA (mRNA) expression and down-regulated Bcl-2 mRNA expression. Together, these responses increased hepatocyte sensitivity to TAA-induced cytotoxicity and forced the damaged cells to undergo apoptosis. Enhancing the tendency of damaged hepatocytes to undergo apoptosis may be the protective mechanism whereby curcumin suppresses inflammatory responses and hepatic fibrogenesis. These results provide a novel insight into the cause of hepatic fibrosis and the cytoprotective effects curcumin has on hepatic fibrosis suppression
机译:炎症和肝星状细胞(HSC)激活是形成肝纤维化最关键的步骤。被病毒或细菌感染,酒精或有毒化学物质损坏的肝细胞会引发炎症反应,从而激活HSC产生的胶原蛋白。最近的研究表明姜黄素具有抗炎,抗氧化和抗癌的作用,因此具有肝脏保护作用。但是,机制尚不清楚。在这项研究中,我们显示姜黄素通过抑制HSC活化,炎症反应和诱导受损肝细胞的凋亡,在体内保护BALB / c小鼠免受肝纤维化。使用硫代乙酰胺(TAA)诱导的肝纤维化动物模型,我们发现姜黄素治疗上调了P53蛋白表达和Bax Messenger RNA(mRNA)表达,并下调了Bcl-2 mRNA表达。这些反应共同提高了肝细胞对TAA诱导的细胞毒性的敏感性,并迫使受损细胞发生凋亡。增强受损肝细胞凋亡的趋势可能是姜黄素抑制炎症反应和肝纤维化的保护机制。这些结果为了解肝纤维化的原因以及姜黄素对抑制肝纤维化的细胞保护作用提供了新颖的见解。

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