木瓜提取物对高糖高脂诱导的小鼠非酒精性脂肪性肝病的影响

Effects of Extracted Active Components of Chaenomeles Speciosa on Non-alcoholic Fatty Liver Disease in Model Mice induced by High-fat–high-fructose Diet

目的观察木瓜提取物对小鼠非酒精性脂肪性肝病(NAFLD)的影响,探讨其可能的分子机制。方法将40只雄性昆明小鼠随机分成正常组、模型组和药物低(50 mg/kg)、高(100 mg/kg)剂量组。正常组给予普通饲料,其他组给予高糖高脂饲养造模,4周后处死,检测体质量、肝脏质量、血清相关指标及肝脏三酰甘油(TG)水平,HE及油红O染色观察肝脏组织形态,RT-PCR和Western blot检测脂代谢相关基因表达。结果与正常组比较,模型组小鼠肝脏明显增大,肝指数明显升高(P<0.01),附睾脂肪指数明显升高(P<0.05);血清丙氨酸氨基转移酶和葡萄糖水平升高(P<0.05);肝脏TG水平升高(P<0.05);病理结果显示,肝脏脂肪变性明显;RT-PCR和Western blot结果显示,模型组肝脏组织SIRT1、FoxO1表达水平下调,SERBP-1c表达水平上调。与模型组比较,药物低、高剂量组脂肪肝病理损伤明显改善,肝指数、肝脏TG含量均下降,SIRT1和FoxO1表达水平上调。结论木瓜提取物对高糖高脂诱导的NAFLD有保护作用,其机制可能是通过SIRT1-FoxO1信号通路发挥作用。

Objective To study the effects of extracted active components of Chaenomeles Speciosa(EACCS)on non-alcoholic fatty liver disease(NAFLD)in mice;To discuss the possible molecular mechanism.Methods Forty male KM mice were randomized into four groups,namely normal group,model group,low-dose(50mg/kg)EACCSgroup and high-dose(100mg/kg)EACCS group.Except that the normal group was daily given routine diet,the other groups were given high-fat–high-fructose diet(HFFD).The mice were put to death4weeks later.Body weight,liverweight and serum TG were measured.HE and oil red O staining were used to observe liver tissue morphology.RT-PCR and Western blot were used to detect the expression of lipid metabolism related genes.Results Compared with the normal group,the liver size,liver index(P<0.01)and epididymal fat index(P<0.05)increased significantly;The ALT and GLU in serum increased(P<0.05),TG increased(P<0.05),and pathological findings showed significantsteatosis;RT-PCR and Western blot showed that the expression levels of SIRT1and FoxO1mRNA decreased and thelevel of SERBP-1c increased in the model group.Compared with the model group,the hepatic lipid accumulation ofEACCS groups was obviously improved,and the serum ALT,GLU,and TG levels significantly decreased,the expression levels of hepatic SIRT1and FoxO1mRNA increased.Conclusion EACCS has protective effects on NAFLD mice induced by HFFD,and its mechanism may be related to the activation of SIRT1-FoxO1signaling pathway in the liver tissues.