摘要
目的:探讨中药复方糖肾方(TSF)调控非酒精性脂肪性肝病(NAFLD)小鼠自噬改善脂质沉积的潜在机制。方法:通过高脂饲料喂养建立NAFLD小鼠模型,造模成功后灌胃TSF,观察给药后各组小鼠的甘油三酯(TG)、总胆固醇(TC)、谷丙转氨酶(ALT)和谷草转氨酶(AST)水平,利用苏木精-伊红(HE)染色、油红O染色观察肝组织脂质沉积,免疫印迹法(Westernblot)检测自噬标记物LC3B-Ⅰ/Ⅱ、自噬底物p62、沉默信息调节因子(SIRT1)及自噬上游关键分子mTOR等的表达。结果:TSF可显著降低NAFLD模型小鼠血清中TG、TC、ALT及AST的水平,明显改善肝脏组织中脂质沉积。Westernblot结果显示TSF显著上调自噬蛋白LC3BⅡ、SIRT1的表达水平,显著降低p-mTOR和p62蛋白的表达水平。结论:TSF显著减轻NAFLD小鼠模型肝脏脂质沉积,其作用机制可能与调控SIRT1、mTOR介导的自噬通路相关。
Objective:To investigate the potential mechanism of the traditional Chinese medicine Tangshen Formula(TSF)in regulating autophagy to improve lipid deposition in a mouse model of non-alcoholic fatty liv-er disease(NAFLD).Methods:NAFLD mouse model was established through high-fat diet feeding.After the model was successfully established,TSF was administered orally.The levels of triglycerides(TG),total cholester-ol(TC),glutamic pyruvic transaminase(ALT),and glutamic oxaloacetic transaminase(AST)in the mice were ob-served after modeling and medication.Hematoxylin-eosin(HE)staining and Oil Red O staining were used to observe lipid deposition in their liver tissues.The expression of key molecules such as autophagy marker LC3B-I/I,autophagy substrate p62,silent information regulator 1(SIRT1),and key upstream molecule mTOR in autophagy were detected by Western blot.Results:TSF significantly reduced the expression levels of TG,TC,ALT,and AST in the serum of NAFLD model mice and significantly improved lipid deposition in the liver tissues.Western blot results showed that TSF significantly upregulated the expression levels of autophagy protein LC3BII and SIRTI and significantly downregulated the expression levels of p-mTOR and p62 pro-teins.Conclusion:TSF significantly alleviated lipid deposition in the liver of the NAFLD mouse model.Its mechanism may be related to the regulation of the autophagy pathway mediated by SIRTI and mTOR.
出处
《中日友好医院学报》
CAS
2023年第6期333-336,349,F0003,共6页
Journal of China-Japan Friendship Hospital
基金
国家自然科学基金(82004328,82174296,82004357)。
关键词
非酒精性脂肪性肝病
糖肾方
脂质沉积
自噬
non-alcoholic fatty liver disease
Tangshen Formula
lipid deposition
autophagy
