摘要Objective: To investigate the intervention effect and specific mechanism of Jisheng Shenqi Decoction plus Panax notoginseng and Turmeric on carbon tetrachloride (CCl4)-induced liver fibrosis in rats. Methods: SPF SD rats were randomly divided into control group, model group, and Chinese medicine treatment (low, medium and high dose) groups. The model group and Chinese medicine treatment group were given intraperitoneal injection of 40％ CCl4 olive oil solution twice a week. A rat model of liver fibrosis was replicated by the method for 8 weeks. After successful modeling, each drug-administered group was gavaged with corresponding drugs, and the control group and model group were gavaged with equal volume of distilled water, once a day, for 4 weeks. After the last intragastric administration, HE staining and Masson staining were used to observe the pathological morphology of liver tissue, and liver function (ALT, AST) was detected; ELISA method was used to determine transforming growth factor β (TGF-β), angiotensin Ⅱ( Ang-Ⅱ), chitinase 3-like protein 1 (CHI3L1), interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) content; The expression levels of type I, type Ⅲ collagen (Col-Ⅰ, Col-Ⅲ) and TGF-β mRNA were determined by RT-PCR. Results: ①HE and Masson staining showed that a large number of liver cells in the model group were inflamed and necrotic, the collagen fibers in the liver tissue were extensively proliferated, the fibrous septa were interconnected, and the pseudolobules were formed. Compared with the model group, the levels of ALT, AST, TGF-β, Ang-Ⅱ, CHI3L1, IL-1, IL-6 and TNF-α in the traditional Chinese medicine treatment group were decreased, while the levels of Col-Ⅰ, Col-Ⅲ The expressions of Ⅲ and TGF-β mRNA were decreased, and the effect was most obvious in the middle and high dose groups of traditional Chinese medicine (P<0.01). Conclusion: Jisheng Shenqi Decoction combined with Panax notoginseng and Biejia can significantly improve liver fibrosis induced by CCl4 in rats, and its mechanism may be related to the down-regulation of angiotensin-converting enzyme (ACE)-angiotensin Ⅱ(Ang-II)-angiotensin Ⅱ receptor 1 (AT1R) signaling pathway related gene expression, reducing the level of related cytokines, promoting the degradation of extracellular matrix and so on.