School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China; Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100005, China.
J Ethnopharmacol. 2024 Jan 30;319(Pt 3):117334. doi: 10.1016/j.jep.2023.117334. Epub 2023 Oct 18.
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 (CCl). 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 CCl-induced rats through multi-pathway regulation. This study provides protein information on liver fibrosis treated with QJ.
七甲柔肝汤（QJ）由八味草药和两种动物药组成，是一种具有保肝和抗纤维化作用的有效中药。然而，其潜在的作用机制尚不清楚。
探讨 QJ 治疗大鼠肝纤维化的作用机制。
采用四氯化碳（CCl）构建纤维化大鼠模型。用 QJ 对纤维化大鼠进行口服给药。采用苏木精-伊红和 Masson 三色染色评估肝组织病理变化。采用定量蛋白质组学分析 QJ 中的差异表达蛋白（DEPs）。随后，采用 Western blot 验证 QJ 治疗后肝纤维化的潜在机制。
QJ 显著改善了肝功能，减轻了纤维化进展。基于串联质量标签（TMT）蛋白质组学，我们在 QJ 与模型组和模型组与对照组之间共鉴定到 818 个共同的 DEPs，包括 296 个上调的和 522 个下调的 DEPs，它们主要参与代谢途径、氧化还原反应和胶原生物合成过程。此外，我们发现 QJ 通过抑制半胱天冬酶蛋白的表达、抑制促凋亡蛋白和促进抗凋亡蛋白来减少肝细胞死亡。我们进一步证实 QJ 抑制了 Akt/mTOR 通路。
QJ 通过多途径调节在 CCl 诱导的大鼠中发挥了保肝作用。本研究为 QJ 治疗肝纤维化提供了蛋白质信息。
