蓝莓对非酒精性脂肪性肝病小鼠肝细胞核因子相关因子2表达的影响

Effect of blueberry compound on hepatocyte expression of Nrf2 in mice model of non-alcoholic fatty liver disease

目的:研究蓝莓对非酒精性脂肪性肝病(NAFLD)小鼠的保护作用及相关机制。方法:40只健康C57BL/6J小鼠随机分为4组:正常组、蓝莓组、姜黄素组、模型组。正常组饲喂正常饲料,其余各组饲喂高脂饲料。蓝莓组每日灌胃蓝莓原浆(15 ml·kg-1·d-1);姜黄素组每日灌胃姜黄素溶液(200mg·kg-1·d-1);其余组小鼠灌胃等体积生理盐水,12周后处死。油红染色观察各组肝脏形态变化;全自动生化分析仪检测血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、三酰甘油(TG)、总胆固醇(TC)含量;酶联免疫法检测肝组织中超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)、丙二醛(MDA)及三酰甘油(TG)含量;Western blot检测小鼠肝组织中核因子相关因子2(Nrf2)蛋白的表达。结果:与模型组小鼠相比,蓝莓组、姜黄素组油红染色肝组织中脂肪沉积明显减少,血清AST、ALT、TG、TC含量明显降低(P<0.05),肝组织中TG、MDA含量明显下降(P<0.05),而SOD活性、GSH含量及Nrf2蛋白表达明显增高(P<0.05)。结论:蓝莓对NAFLD有较好的防治作用,其机制可能与上调肝组织中Nrf2的表达,提高机体抗氧化能力相关。

Objective： To investigate the effect of blueberry on non-alcoholic fatty liver disease in mice and its mechanism. Methods：Forty healthy C57 BL /6J mice were randomly divided into normal control group,blueberry group,Curcumin group and model group. The mice in normal control group were given normal diet,those in other groups were all given high fat diet. At the same,blueberry group were intragastrically given blueberry juice（ 15 ml · kg- 1·d- 1）,Curcumin group were gavaged Curcumin solution（ 200mg·kg- 1·d- 1）,those in other groups were gavaged with physiological saline daily. At the end of week 12 all mice were sacrificed. Pathological changes in the hepatic tissue by oil red staining,the level of alanine aminotransferase（ ALT）,aspartate aminotransferase（ AST）,triglyceride（ TG） and total cholesterol（ TC） in serum were detected by automatic biochemical analyze. The hepatic TG,TC levels,MDA contents,GSH levels and SOD activity were quantified by ELISA. The expression of nuclear factor-E2-related factor 2（ Nrf2） in liver tissue was detected by Western blot. Results： Compared to model group,blueberry group liver showed decreased lipid accumulation,serum ALT,AST,TG and TC levels decreased（ P 0. 05）,The hepatic TG,MDA also decreased（ P 0. 05）,while GSH contents,SOD activity and the expression of Nrf2 levels increased（ P 0. 05）.Conclusion： Blueberry possessed a protective effect on non-alcoholic fatty liver disease in mice,the mechanism might be associated with upregulating the expression of hepatic Nrf2.