蛋白激酶B
纤维化
肝纤维化
医学
PI3K/AKT/mTOR通路
四氯化碳
药理学
四氯化碳
细胞凋亡
蛋白质组学
下调和上调
化学
癌症研究
病理
生物化学
有机化学
基因
作者
Xiaofeng Chen,Xin Sun,Shaoxiu Ji,Yu Han,Peijie Wu
标识
DOI:10.1016/j.jep.2023.117334
摘要
Qijia Rougan decoction (QJ), consisting of eight herbs and two animal drugs, is an effective traditional Chinese medicine with hepatoprotective and antifibrotic effects. However, its underlying action mechanism remains unclear. To explore the mechanism underlying the treatment of liver fibrosis in rats by QJ. Rats with fibrosis were constructed using carbon tetrachloride (CCl4). The QJ was orally administered to fibrotic rats. Hepatic pathological changes were evaluated using hematoxylin and eosin and Masson's trichrome staining. The differentially expressed proteins (DEPs) in QJ were analyzed using quantitative proteomics. Subsequently, the underlying mechanisms in liver fibrosis after QJ treatment were validated using Western blotting. The QJ markedly improved liver function and attenuated fibrotic progression. Based on the tandem mass-tag based (TMT) proteomics, we identified 818 common DEPs between QJ vs Model and Model vs Control, including 296 upregulated and 522 downregulated DEPs, which mostly participate in metabolic pathways, oxidation-reduction reactions, and collagen biosynthetic processes. In addition, we found that QJ reduced hepatocellular death by inhibiting the expression of caspase proteins, repressing pro-apoptotic proteins, and promoting anti-apoptotic proteins. We further demonstrated that QJ suppressed the Akt/mTOR pathway. QJ exerted hepatoprotective effects in CCl4-induced rats through multi-pathway regulation. This study provides protein information on liver fibrosis treated with QJ.
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