陈芝芸;温秀梅;严茂祥;何蓓晖;
CHEN Zhiyun*,WEN Xiumei,YAN Maoxiang,HE Beihui (Zhejiang Traditional Chinese Medicinal Hospital,Hangzhou 310006,China)

• 1:浙江省中医院消化病研究室

摘要(Abstract)：

目的:观察解偶联蛋白2(UCP2)在高脂饮食诱导的非酒精性脂肪性肝炎(NASH)大鼠肝组织的表达及山楂叶总黄酮(TFHL)对其的影响。方法:以高脂饮食喂养12周诱导SD大鼠建立NASH模型,同时分别以250,125 mg.kg-1.d-1的TFHL和195.4 mg.kg-1.d-1的易善复进行干预,观察大鼠肝组织的病理改变,血清ALT,AST水平,肝组织匀浆TG,CHOL,MDA含量和T-AOC的活性,RT-PCR检测UCP2基因mRNA在肝组织中表达,ELISA检测肝组织UCP2含量。结果:NASH模型组大鼠肝组织重度脂肪变、炎细胞浸润,血清ALT,AST水平和肝组织TG,CHOL,MDA,UCP2含量较正常大鼠明显增高,UCP2 mRNA表达显著增强,T-AOC活性明显降低。肝组织UCP基因的表达与MDA含量呈明显正相关,与T-AOC活性则呈负相关。TFHL高、低剂量组大鼠肝组织炎症活动程度、肝匀浆MDA和UCP2含量以及肝组织UCP2 mRNA表达均较模型组大鼠显著降低,而肝匀浆T-AOC的活性则较模型组大鼠明显增高。结论:TFHL可能是通过抑制氧应激/脂质过氧化反应和肝组织UCP2过表达的途径减轻肝脏炎症损伤,从而防止NASH的进一步发展。
Objective: To study the expression of uncoupling protein 2(UCP2) in liver of rats with nonalcoholic steatohepatitis(NASH) induced by fat-rich diet,and the effect of total flavones of hawthorn leafon(TFHL) on UCP2.Method: The NASH model of rat was induced by 12 weeks of fat-rich diet.Subsequently the rats were administrated with TFHL in accordance with 250,125 mg·kg-1·d-1 and the Essentiale N with 195.4 mg·kg-1·d-1.The change of liver pathological.The levels of serum ALT and AST,the content of TG,CHOL,MDA and T-AOC activity of liver and were evaluated.The UCP2mRNA expression in liver was detected with RT-PCR,and the contents of UCP2 were examined with ELISA.Result: There are severe steatosis,inflammatory cellular infiltration in the liver of the NASH models.The levels of serum ALT,AST and the contents of TG,CHOL,MDA and UCP2 in the model group were higher than those of in the normal groop.The expression of UCP2mRNA was obviously enhanced and the activity of T-AOC decreased.The expression of UCP2 mRNA of rats was positively correlation with the contents of MDA,TNF-α.The inflammation activity in rat liver,the contents of MDA and UCP2,the expression of UCP2 mRNA in the administrated groups were obvously lower than those in the model group,while the activity of T-AOC was higher than that of model.Conclusion: TFHL may alleviate liver injury by means of the suppression of Oxidative stress/lipid peroxidation reaction and the overexpression of UCP2 in liver,which could prevent the further development of NASH.

关键词(KeyWords)： 山楂叶总黄酮;非酒精性脂肪性肝炎;解偶联蛋白2
TFHL;NASH;uncoupling protein

Abstract:

Keywords:

基金项目(Foundation): 浙江省自然科学基金项目(Y2004310)

作者(Author): 陈芝芸;温秀梅;严茂祥;何蓓晖;
CHEN Zhiyun*,WEN Xiumei,YAN Maoxiang,HE Beihui (Zhejiang Traditional Chinese Medicinal Hospital,Hangzhou 310006,China)

Email:

DOI:

参考文献(References)：

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