| 引用本文:王妮华1，3，王琼熠1，3，范辉1，2，3.黄连碱改善脂肪肝SD大鼠模型的效应及机制研究[J].世界中医药,2019,(01):. |
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| 黄连碱改善脂肪肝SD大鼠模型的效应及机制研究 |
| Study on Improvement Effects of the Coptisine on the Fatty Liver Disease of SD Rats and the Related Mechanism |
| 投稿时间：2018-12-10 |
| DOI：10.3969/j.issn.1673-7202.2019.01.010 |
| 中文关键词: 黄连碱 脂肪肝 AMP AMPK |
| English Keywords:Coptisine Fatty liver AMP AMPK |
| 基金项目:广东省科技厅实验室建设项目（2017B030314064） |
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| 中文摘要: |
| 目的：观察黄连碱对脂肪肝SD大鼠模型脂代谢指标的影响，探讨作用机制。方法：采用高脂饲养构建SD大鼠脂肪肝模型，随机分组为正常对照组、高脂模型组、黄连碱低、高剂量组（10 mg/kg、50 mg/kg），给药30 d，分析大鼠体重、肝指数、三酰甘油（TG）、肝功能（ALT，AST）及肝脏病理等指标；采用人肝癌HepG2细胞系，蛋白免疫印迹法（WB）观察黄连碱对AMP-活化蛋白激酶（AMPK）蛋白的表达，反转录荧光定量PCR（RT-PCR）方法分析肉碱脂酰转移酶1（CPT-1）mRNA、羟甲基戊二酰辅酶A（HMG-Coa）mRNA的表达，高效液相色谱（HPLC）测定细胞内AMP的含量。结果：与高脂饮食组比较，黄连碱低、高剂量组均降低了TG水平、改善AST以及肝脏组织学形态，且黄连碱高剂量组效果优于低剂量组。在HepG2细胞中，黄连碱显著提高AMP的浓度，激活AMPK蛋白磷酸化表达，上调CPT-1 mRNA的表达，抑制HMG-Coa mRNA的表达。结论：黄连碱具有显著改善大鼠脂肪肝的效应，作用机制可能与提高AMP的浓度，激活AMPK信号通路有关。 |
| English Summary: |
| To observe the effect of coptisine on the fatty liver disea-se of SD (Sprague Dawley) rats and investigate the mechanism. Methods:The SD fatty liver rats were induced by high fat diet. Rats were randomly divided into normal control group，high fat model group，coptisine low and high dose groups (10 mg/kg or 50 mg/kg). After 30 days of administration，the body weight，liver index，triglyceride (TG)，liver function (alanine transaminase (ALT)，aspartate aminotransferase (AST) and liver pathology of each group were analyzed. The expression of coptisine to adenosine monophosphate activated protein kinase (AMPK) protein in human HepG 2 cell line was estimated by Western Blot (WB)，the expression of carnitine palmitoyltransferase-1 messenger Ribose Nucleic Acid (CPT-1 mRNA) and hydroxy-methylglutaryl coenzyme A messenger Ribose Nucleic Acid (HMG-CoA mRNA) was analyzed by Real Time-Poly Polymerase Chain Reaction (RT-PCR)，and the content of adenosine monophosphate (AMP) in the cell was determined by high performance liquid chromatography (HPLC). Results:Compared with the high-fat diet group，the two groups of coptisine intervention reduced the TG level of blood lipid，AST，and triglyceride content in liver，and significantly improved the histological morphology of liver in high-fat feeding. The high-dose group was better than the low-dose group. The HepG2 cells were treated with coptisine，AMP concentration was significantly increased，the activation of AMPK protein phosphorylation was increased，the expression of CPT-1 mRNA expression was also increased，and the expression of HMG-CoA mRNA was inhibited (P<0.05). Conclusion:The coptisine can remarkably improve fatty liver in rats，and its mechanism may be related to the increasing of AMP concentration and the activation of AMPK signaling pathway. |
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