黄连解毒汤对高脂血症小鼠肝脏保护作用的观察

作者	单位	E-mail
马雅銮,李彤,王蓓蓓
曾辉	首都医科大学附属北京地坛医院传染病研究所（北京 100011）	zenghui@ccmu.edu.cn

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中文摘要:

目的观察黄连解毒汤对高脂饮食导致的载脂蛋白E（apolipoprotein E，ApoE）基因敲除（ApoE－/－）小鼠肝脏损伤的保护作用。方法野生型小鼠分为野生普食组、野生高脂组，ApoE－/－小鼠分为ApoE－/－普食组、ApoE－/－高脂组、ApoE－/－高脂加中药组，每组5只，分别给予普食和高脂饮食4周。ApoE－/－高脂加中药组同时给予黄连解毒汤5 g/（kg·d）灌胃。检测小鼠血浆总胆固醇（TC）、甘油三酯（TG）和低密度脂蛋白胆固醇（LDL-C）水平，HE染色观察肝脏病理组织变化，流式细胞仪检测肝脏巨噬细胞及其亚型比例和巨噬细胞表面受体CD206、CD36表达水平。结果 ApoE－/－高脂组小鼠肝脏组织呈典型单纯性脂肪肝病理变化，TC、TG、LDL-C升高，巨噬细胞比例增多，巨噬细胞表面受体CD206表达水平降低，与ApoE－/－普食组比较，差异均有统计学意义（P<0.01， P<0.05）；CD206+替代活化型（alternatively activated macrophages，M2型）巨噬细胞比例较野生普食组显著减少（P<0.05）；CD36表达水平无明显变化。黄连解毒汤干预4周后，血脂无明显改善，但肝脏CD206+M2型巨噬细胞比例较ApoE－/－高脂组显著提高（P<0.05），肝脏脂肪肝病理变化显著减轻。结论黄连解毒汤的肝脏保护功能可能与M2型巨噬细胞免疫调节、修复损伤组织有关，其免疫调节作用和肝脏保护作用独立于降脂作用。

英文摘要:

Objective To observe the protection of Huanglian Jiedu Decoction （HJD） on high fat diet induced liver damage mice ［hyperlipidemic mice lacking apolipoprotein E （ApoE－/－）］. Methods Wild type mice were divided into the wild common food group and the wild hyperlipidemia group. ApoE－/－mice were divided into the ApoE－/－common food group， the ApoE－/－ hyperlipidemia group， and the ApoE－/－ hyperlipidemia plus HJD group， 5 in each group. In the present study， wild type mice and homozygous apoE－/－ mice were fed with a chow diet or a high cholesterol Western diet for 4 weeks. HJD at the daily dose of 5 g/kg was given to mice in the ApoE－/－ hyperlipidemia plus HJD group by gastrogavage. The plasma levels of total cholesterol （TC）， triglyceride （TG）， low density cholesterol protein （LDL-C） were detected. The pathohistological changes of the liver were observed by Eosin and Hematoxylin （HE） staining. The liver macrophages and their subtype ratios， as well as macrophage surface receptor CD206 and CD36 were detected by flow cytometry. Results Typical pathological changes of simple fatty liver were manifested in the ApoE－/－ hyperlipidemia group， TC， TG， and LDL-C increased， the macrophage ratio increased， the expression level of macrophage surface receptor CD206 decreased， showing statistical difference when compared with the ApoE－/－common food group （P<0.01， P<0.05）. The ratio of alternatively activated macrophages （M2） subpopulations was lower in the ApoE－/－ hyperlipidemia group than in the wild common food group （P<0.05）. There was no obvious change in the expression level of CD36. After intervened by HJD for 4 weeks， there was no obvious improvement in blood lipids. But the ratio of CD206+M2 macrophages was significantly improved， when compared with the ApoE－/－ hyperlipidemia group （P<0.05）. The pathological changes of fatty liver were significantly attenuated. Conclusions The liver protection effect of HJD might be associated with immunoregulation of M2 macrophage subpopulations and injured tissue repairment. Its immunoregulation and liver protection were independent from lipids lowering.

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