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目的探讨血管紧张素转化酶抑制剂(ACEI)依那普利(Ena)对大鼠肝纤维化的防治作用及其部分机制,及对肝组织bax和bcl-2基因表达的影响。方法以四氯化碳(CCl_4)诱导形成大鼠肝实质损伤性肝纤维化模型。大鼠分为空白对照组、模型对照组、预防组及治疗组。除空白对照组外,其余各组大鼠均皮下注射40％CCl_4橄榄油混合液,每3日1次,共10周。预防组同时给予Ena灌胃。治疗组则在造模第5周给予Ena灌胃。对肝组织标本炎症及纤维化程度进行评价,并用RT-PCR技术观察Ena对肝组织bax和bcl-2基因表达的影响。结果Ena高剂量预防及高剂量治疗组肝组织炎症和纤维化程度较模型对照组显著减轻(P＜0．01)。Ena高剂量预防及高剂量治疗组肝组织bax基因表达显著弱于模型对照组(P＜0．01),bcl-2基因表达显著强于模型对照组(P＜0．01),bax/bcl-2基因表达比值和肝纤维化程度呈显著直线正相关(P＜0．01)。结论Ena能有效防治大鼠肝纤维化,抑制促凋亡基因bax的表达,促进抑凋亡基因bcl-2的表达,是其可能机制之一。bax/bcl-2基因表达比值与肝纤维化程度正相关。
Objective To investigate the prevention and treatment of angiotensin converting enzyme inhibitor (Ena) on hepatic fibrosis in rats and its mechanism and its effect on the expression of bax and bcl-2 in liver tissue. Methods Carbon tetrachloride (CCl 4) induced hepatic fibrosis model in rats. Rats were divided into blank control group, model control group, prevention group and treatment group. Except for the blank control group, the rest of the rats in each group were subcutaneously injected 40% CCl_4 olive oil mixture once every three days for 10 weeks. Prevention group also given Ena gavage. The treatment group was given intragastric Ena 5 weeks after modeling. The degree of inflammation and fibrosis in liver tissue specimens were evaluated, and the effect of Ena on the expression of bax and bcl-2 genes in liver tissue was observed by RT-PCR. Results Ena high-dose prophylaxis and high-dose treatment group liver inflammation and fibrosis than the model control group significantly reduced (P <0.01). The expression of bax gene in liver tissue of Ena group was significantly lower than that of model control group (P <0.01), the expression of bcl-2 gene was significantly higher than that of model control group (P <0.01), bax / bcl -2 gene expression and the degree of liver fibrosis showed a significant positive correlation (P <0.01). Conclusion Ena can effectively prevent and treat hepatic fibrosis, inhibit the expression of pro-apoptotic gene bax and promote the expression of apoptosis-inhibiting gene bcl-2, which may be one of its possible mechanisms. The ratio of bax / bcl-2 gene expression was positively correlated with the degree of liver fibrosis.