| 摘 要： | Objective: To explore the effect of Biejiajian Oral Liquid(鳖甲煎口服液, BOL) on CCl4-induced hepatic fibrosis in rats by detecting the changes in the levels of angiotensinⅡ(AngⅡ), angiotensin-(1–7) [Ang-(1–7)], angiotensin-converting enzyme(ACE), ACE2, angiotensinⅡ type 1 receptor(AT1 R), Mas, etc. Methods: A total of 180 Wistar rats were randomly divided into two groups by random digital table method: prevention experiment and treatment experiment. Each group was further subdivided into the fol owing 6 subgroups: normal control group, model group, vitamin E [100 mg/(kg·d), VE] group, enalapril [10 mg/(kg·g), Ena] group, high-dosage [20 g/(kg·d)] BOL group, and low-dosage [10 g/(kg·d)] BOL group. The hepatic fibrosis rat model was established by subcutaneous injection of CCl4 for 6 weeks. Prevention experiment and treatment experiment were administered with specific drugs at different times. At the end of treatment experiment, the pathological changes of liver were observed after hematoxylin-eosin staining. The expressions of ingredients in renin-angiotensin-aldosterone system(RAAS) such as AngⅡ, Ang-(1–7), ACE, ACE2, AT1 R, Mas, renin, CYP11 B2 and angen in liver were detected by enzyme linked immunosorbent assay, immunohistochemistry method or reverse transcription-polymerase chain reaction, respectively. Results: The levels of AngⅡ and Ang-(1–7) at the 6 th week increased by 496.10% and 73.64%, respectively, compared with those at the 2 nd week in the model group(P0.01). With prevention or treatment with high-dosage BOL, there was an evident reduction of AngⅡ level but an improvement of Ang-(1–7) level. Specifically, AngⅡ level of high-dosage group decreased by 77.50% in prevention experiment(P=0.000) and by 76.93% in treatment experiment(P=0.002) compared with that in the model group. Ang-(1–7) level increased by 91.69% in prevention experiment(P=0.006) and by 70.77% in the treatment experiment(P=0.010) compared with that in the model group. The expression levels of m RNA of renin, ACE, CYP11 B2, angen and AT1 R decreased by 58.15%, 99.90%, 99.84%, 99.99% and 99.99%(al P0.01), respectively. Conclusions: BOL could help resist liver fibrosis in rats by enhancing the level of each ingredient in ACE2-Ang-(1–7)-Mas axis, while decreasing the level of each ingredient in ACE-AngⅡ-AT1 R axis. To some extent, BOL could enhance the regulation of RAAS in rats with CCl4-induced hepatic fibrosis.
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