阿托伐他汀对非酒精性脂肪性肝病大鼠脂肪细胞因子的影响

中国临床药理学与治疗学 ›› 2015, Vol. 20 ›› Issue (5): 520-524.

阿托伐他汀对非酒精性脂肪性肝病大鼠脂肪细胞因子的影响

陆永娟, 陈芝芸, 严茂祥, 何蓓晖, 朱丹

浙江中医药大学第一临床医学院浙江省中医院,杭州 310006,浙江

收稿日期:2014-09-11 修回日期:2015-02-02 发布日期:2015-06-11
通讯作者: 陈芝芸,女,研究员,博士生导师,研究方向:中医药防治消化系统疾病。Tel: 0571-87071380 E-mail: zhiych123@163.com
作者简介:陆永娟,女,硕士研究生,研究方向:中医药防治消化系统疾病。Tel: 15858111891 E-mail: 734479153@qq.com
基金资助:
浙江省自然科学基金(Y2100170)

Effect of atorvastatin on adipokines in rats with nonalcoholic fatty liver disease

LU Yong-juan, CHEN Zhi-yun, YAN Mao-xiang, HE Bei-hui, ZHU Dan

The 1st Clinical Medical College of Zhejiang TCM University, Zhejiang Provincial Hospital of TCM, Hangzhou 310006,Zhejiang,China

Received:2014-09-11 Revised:2015-02-02 Published:2015-06-11

摘要/Abstract

摘要： 目的: 探讨阿托伐他汀对高脂饮食诱导的非酒精性脂肪性肝病(NAFLD)大鼠脂肪细胞因子脂联素、内脂素、抵抗素的影响。方法: 采用高脂饮食10周建立NAFLD大鼠模型,同时以阿托伐他汀进行干预;生化法检测肝组织甘油三酯(TG)和胆固醇(CHOL)含量,HE染色光镜观察肝组织脂肪变和炎症程度,计算NAFLD活动度积分(NAS);ELISA法检测脂联素、内脂素和抵抗素水平,实时荧光定量PCR检测肝组织脂联素、内脂素、抵抗素基因的mRNA表达。结果: 模型组大鼠肝组织NAFLD活动度积分和TG、CHOL含量较正常组明显增高(P<0.01),脂联素血清含量及肝组织mRNA表达较正常组明显降低(P<0.01),而内脂素、抵抗素血清含量及肝组织mRNA表达均较正常组显著增强(P<0.01);应用阿托伐他汀干预后,肝组织病理学改善,肝脏TG、CHOL含量较模型组明显降低(P<0.05),脂联素血清含量及肝组织mRNA表达水平较模型组增高(P<0.05),内脂素、抵抗素血清含量及肝组织mRNA表达则均较模型组显著下降(P<0.05)。结论: 高脂饮食诱导的NAFLD存在脂联素、内脂素、抵抗素等炎症因子分泌的紊乱,阿托伐他汀可能通过降低脂质在肝脏沉积,上调脂联素,抑制内脂素、抵抗素的过表达,从而抑制肝细胞炎症,防止NAFLD的进展。

关键词: 阿托伐他汀, 非酒精性脂肪性肝病, 脂联素, 内脂素, 抵抗素

Abstract: AIM: To observe the effect of atorvastatin on such adipokines as adiponectin, visfatin and resistin in rats with nonalcoholic fatty liver disease induced by high fat diet.METHODS: The NAFLD model was induced by 10 weeks of high fat diet, then they were intragastrically administrated with atorvastatin. The levels of hepatic TG and CHOL in NAFLD rats were detected by biochemical test. The hepatic steatosis and inflammation were observed with HE staining, the NAFLD activity score(NAS) was counted. The levels of hepatic adiponectin, visfatin and resistin were detected by EL-ISA, the hepatic mRNA expression levels of adiponectin, visfatin and resistin were detected by Realtime PCR.RESULTS: The NAS and levels of hepatic TG and CHOL in model rats were significantly higher than those of normal group (P<0.01), the levels of serum adiponectin and hepatic mRNA expression in NAFLD rats were significantly decreased compared with the normal group (P<0.01), while the levels of visfatin , resistin and their mRNA expression were significantly increased compared with the normal group (P<0.01). After intervention with atorvastatin, the pathology of liver tissue improved, the levels of hepatic TG, CHOL were significantly lower than those of model group (P<0.05), the levels of serum adiponectin and hepatic mRNA expression in NAFLD rats liver were increased compared with the modle group (P<0.05), while the levels of serum visfatin, resistin and hepatic mRNA expression were decreased compared with the model group (P<0.05).CONCLUSION: Disorders of secretion of such inflammatory factors as adiponectin, visfatin and resistin emerge in NAFLD induced by high fat diet. With reducing the deposition of lipids in the liver, raising the expression of adiponectin, inhibiting the overexpression of visfatin and resistin, atorvastatin may inhibit inflammation reaction of hepatocytes , prevent NAFLD progress.

Key words: atorvastatin, nonalcoholic fatty liver disease, adiponectin, visfatin, resistin

中图分类号:

R965.2

陆永娟, 陈芝芸, 严茂祥, 何蓓晖, 朱丹. 阿托伐他汀对非酒精性脂肪性肝病大鼠脂肪细胞因子的影响[J]. 中国临床药理学与治疗学, 2015, 20(5): 520-524.

LU Yong-juan, CHEN Zhi-yun, YAN Mao-xiang, HE Bei-hui, ZHU Dan. Effect of atorvastatin on adipokines in rats with nonalcoholic fatty liver disease[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2015, 20(5): 520-524.

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