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作 者:李金霞[1] 穆凌云[1] 张秋云[1] 陈煜[2] 高连印[1] 杜宇琼[1]
机构地区:[1]首都医科大学中医药学院、中医络病研究北京市重点实验室,北京100069 [2]首都医科大学附属佑安医院人工肝中心,北京100069
出 处:《中国中医药信息杂志》2016年第4期45-48,共4页Chinese Journal of Information on Traditional Chinese Medicine
基 金:首都中医药研究专项(14ZY01)
摘 要:目的动态观察截断逆挽方对慢加急性肝衰竭(ACLF)大鼠线粒体凋亡途径的影响,探讨其作用机制。方法 SPF级Wistar大鼠随机分为正常组、模型组和截断逆挽方组,猪血清腹腔注射13周联合D-氨基半乳糖、脂多糖急性攻击建立ACLF模型。截断逆挽方组在急性攻击前予截断逆挽方灌胃3 d。各组大鼠于急性攻击后4、8、12 h平行取材。电镜观察肝细胞超微结构,免疫组化检测肝组织细胞色素C(Cyt C)表达,Western blot检测肝组织Bid蛋白表达。结果与正常组比较,模型组4、8 h Cyt C和Bid表达量增加、12 h表达量减少(P<0.05);与模型组比较,截断逆挽方组4、8 h Cyt C和Bid表达量减少、12 h表达量增加(P<0.05)。电镜观察显示,模型组大鼠肝细胞超微结构严重破坏,且程度逐渐加深,而各时间点截断逆挽方组大鼠肝细胞超微结构损伤程度较模型组均有所减轻。结论截断逆挽方可有效降低ACLF大鼠肝细胞的损伤程度,其作用机制可能与阻断肝细胞线粒体凋亡途径有关。ObjectiveTo dynamically observe the effects ofJieduan Niwan Formula on mitochondrial apoptotic pathway in acute-on-chronic liver failure (ACLF) rats; To further reveal the possible mechanism ofJieduan Niwan Formula.MethodsSPF Wistar rats were randomly divided into normal group, model group andJieduan Niwan group. 13-week porcine serum injection followed withD-galactosamine and lipopolysaccharide joint acute attack was used to established ACLF model in all rats except for normal group. Rats inJieduan Niwangroup were orally givenJieduan NiwanFormula for 3 days before acute attack. Rats were sacrificed respectively at 4, 8 and 12 h after models were established. The expressions of Bid, Cytochrome C (Cyt C) and hepatocyte ultrastructure were detected by Western blot method, immunohistochemical analysis and transmission electron microscope, respectively.Results Compared with normal group, the levels of Cyt C and Bid in model group increased at 4 h and peaked at 8 h but decreased at 12 h (P<0.05); however, the levels of Cyt C and Bid inJieduan Niwan group were lower than those in model group at 4 and 8 h but higher at 12 h (P<0.05). The ultrastructures were significantly damaged in model rats, which severity was escalated through time; inJieduan Niwan group, the degree of injury decreased at each timing.ConclusionJieduan NiwanFormula can efficiently alleviate the hepatocyte damage in ACLF rats, and the mechanism might be involved in the inhibition of the mitochondrial apoptotic pathway.
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