【摘要】 目的:探讨白背叶根(MMAR)水提物对四氯化碳(CCl4)诱导大鼠肝纤维化的保护机制。方法:将大鼠随机平均分为6组:对照组,模型组,秋水仙碱组(0.2mg/kg),MMAR高、中、低剂量组(分别相当于生药5、2.5、1.25g/kg),每组12只,对照组和模型组给予等量0.9%氯化钠溶液。实验结束后,采集血液和肝脏。使用全自动生化分析仪检测大鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)水平;试剂盒检测血清中超氧化物歧化酶(SOD)、丙二醛(MDA)、羟脯氨酸(Hyp)水平;HE和Masson染色观察肝脏病理学改变;q-PCR测定Col-Ⅰ、TIMP-1、TGF-β1、α-SMA mRNA表达。结果:与模型组比较,MMAR各剂量组血清中ALT、AST、MDA和Hyp的水平明显降低(P<0.05),SOD活性明显升高(P<0.05),NMAR高、中剂量组Col-Ⅰ、TIMP-1、TGF-β1、α-SMA mRNA表达被显著抑制(P<0.05)。结论:MMAR可以通过抑制氧化应激、恢复MMPs和TIMPs之间的平衡、抑制HSC活化等途径显著减轻CCl4诱导的肝纤维化。更多还原

【Abstract】 Objective: To investigate the protective effect of water extract of Mallotus apeltan(Lour.) Muell.-Arg. root(MMAR) on CCl4-induced hepatic fibrosis, exploring the underlying mechanism of MMAR against liver fibrosis. Methods: Rats were randomly divided into six groups(12 in each group): normal control group, model group, colchicine group(0.2 mg/kg), MMAR high-, medium-, low-dose treatment group(5, 2.5, 1.25 g/kg). The rats in normal control group and model group were given equivalent 0.9% sodium chloride solution. At the end of the experiment, the blood and liver samples were collected for the further examination. The levels of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) in serum were detected by using an automatic biochemical analyzer. The levels of superoxide dismutase(SOD), malondialdehyde(MDA), and hydroxyproline(Hyp) in serum were detected by commercial assay kits. The hepatic histopathological changes were observed by HE and Masson staining. Additionally, the mRNA expression of Col-Ⅰ, TIMP-1, TGF-β1 and α-SMA were measured by real-time quantitative PCR. Results: Compared with the model group, treatment with MMAR could significantly decrease the levels of ALT, AST, MDA and Hyp(P<0.05), meanwhile SOD was significantly increased(P<0.05). The mRNA expressions of liver fibrosis biomarkers including Col-Ⅰ, TIMP-1, TGF-β1 and α-SMA in high, medium-dose treatment group were significantly decreased(P<0.05). Conclusion: MMAR significantly alleviates CCl4-induced hepatic fibrosis by inhibiting oxidative stress, restoring the balance between MMPs and TIMPs, and suppressing HSC activation.更多还原