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目的观察三七皂苷R1(R1)对ApoE~(-/-)小鼠肝脏白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和微小RNA-146a(miR-146a)的影响。方法采用高脂饲料喂养雄性ApoE~(-/-)小鼠,建立小鼠动脉粥样硬化(Atherosclerosis,AS)模型,随机分为模型组,R1低、中、高剂量组,辛伐他汀组,另设同龄C57BL/6J雄性小鼠为正常对照组。连续给药12周后处死小鼠,检测血糖、血脂、肝功能(AST,ALT)以及肝匀浆TNF-α、IL-6等指标,HE染色观察肝组织病理形态学,PCR测肝脏miR-146a表达。结果模型组小鼠血糖、血脂、ALT、AST、TNF-α、IL-6均较正常对照组显著升高(P<0.05,P<0.01),血清HDL-C含量显著降低(P<0.01),肝脏切片可见小鼠肝细胞质内充满脂滴,大部分肝细胞呈现脂肪变性;与模型组比较,R1高剂量组能显著降低小鼠空腹血糖、血脂、AST、ALT以及肝脏中的TNF-α、IL-6(P<0.01),同时升高HDL-C和miR-146a水平(P<0.01);R1各组小鼠肝脂肪变性较模型组有所减轻。结论三七皂苷R1能降低AS小鼠血糖、血脂水平,并保护肝功能,其机制可能主要与三七皂苷R1升高肝脏miR-146a水平,降低TNF-α、IL-6等炎症因子有关。
Objective To observe the effects of notoginsenoside R1 (R1) on the levels of interleukin-6, tumor necrosis factor-α (TNF-α) and microRNA-146a (miR-146a) in liver of ApoE ~ (- influences. Methods Atherosclerosis (AS) model was established in male ApoE ~ (-) - mice with high fat diet. The mice were randomly divided into model group, low, middle and high dose of R1 group, simvastatin group The same age C57BL / 6J male mice as normal control group. The mice were sacrificed 12 weeks after the continuous administration, blood glucose, blood lipids, liver function (AST, ALT) and liver homogenate TNF-α, IL-6 and other indicators were detected, histopathology of liver was observed by HE staining, 146a expression. Results The levels of blood glucose, blood lipids, ALT, AST, TNF-α and IL-6 in model group were significantly higher than those in normal control group (P <0.05, P <0.01) , Liver sections showed lipid droplets in liver cytoplasm, most of the hepatocytes showed steatosis. Compared with the model group, R1 high-dose group could significantly reduce fasting blood glucose, blood lipid, AST, ALT and liver TNF- α , IL-6 (P <0.01), and elevated the levels of HDL-C and miR-146a (P <0.01). The hepatic steatosis of mice in each group was alleviated compared with the model group. Conclusion Notoginsenoside R1 can reduce blood glucose and blood lipid level and protect liver function in AS mice. The mechanism may be related to the elevation of liver miR-146a and the reduction of inflammatory factors such as TNF-α and IL-6.