生脉散对2型糖尿病大鼠心肌氧化应激的作用及miR-19a、PPARα、CD36因子的影响  

Effects of Shengmai San on myocardial oxidative stress and miR-19a, PPARα, CD36 in type 2 diabetic rats

作　　者：李莺莺 王卫 王欣 王芙蓉 LI Ying-ying;WANG Wei;WANG Xin;WANG Fu-rong(Shandong University of Traditional Chinese Medicine,Jinan 250355,China)

机构地区：[1]山东中医药大学,济南250355 [2]山东中医药大学中医学院

出　　处：《中华中医药杂志》2022年第4期2218-2222,共5页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：山东省自然科学基金项目(No.ZR2020MH387);国家自然科学基金项目(No.82174163)。

摘　　要：目的:观察生脉散对2型糖尿病(T2DM)大鼠心肌组织氧化应激的影响并探讨其作用机制。方法:采用SD大鼠建立T2DM模型。将造模成功大鼠随机分为模型组(n=15)和生脉散组(n=15),另设正常组(n=10)。正常组与模型组均给予蒸馏水灌胃,生脉散组给予生脉散灌胃。给药10周后取大鼠心肌检测氧化应激标志物丙二醛(MDA)水平、超氧化物歧化酶(SOD)与谷胱甘肽过氧化物酶(GSH-Px)活性;同时测定大鼠心肌组织miR-19a水平及过氧化物酶体增殖剂激活受体α(PPARα)和脂肪酸转位酶簇决定因子36(CD36)表达量。结果:与正常组比较,模型组大鼠心肌MDA含量及PPARα、CD36水平显著升高(P<0.01),SOD、GSHPx活性及miR-19a水平显著降低(P<0.01);与模型组比较,生脉散组MDA含量及PPARα、CD36表达量显著下降(P<0.01,P<0.05),SOD、GSH-Px活性及miR-19a水平显著升高(P<0.01)。结论:生脉散可有效改善T2DM大鼠心肌氧化应激反应,该作用可能与影响miR-19a水平进而调控PPARα/CD36信号通路有关。Objective:To observe the effects of Shengmai San(SMS)on oxidative stress of myocardial tissue in type 2 diabetes mellitus(T2DM)rats and explore its mechanism.Methods:SD rats were used to establish T2DM model.Diabetic rats were randomly divided into DM group(n=15)and SMS group(n=15),and blank rats were NC group(n=10).The rats in NC group and DM group were given distilled water,and the SMS group was given SMS.After drug administration for 10weeks,the malondialdehyde(MDA)levels,activity of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)were detected in the myocardium of rats.The cardiac miRNA-19a level,the expression of peroxisome proliferator-activated receptorα(PPARα)and cluster determinant 36(CD36)were also determined.Results:Compared with NC group,MDA content and levels of PPARαand CD36 in myocardium of DM group were significantly increased(P<0.01),while the activity of SOD,GSH-Px and the level of miR-19a were significantly decreased(P<0.01).Compared with DM group,the MDA content and the expressions of PPARαand CD36 in SMS group were significantly decreased(P<0.01,P<0.05),the activity of SOD,GSHPx and the level of miR-19a in myocardium of SMS group were significantly increased(P<0.01).Conclusion:SMS obviously improves oxidative stress in T2DM rats,which may be related to the regulation of PPARα/CD36 signaling pathway by affecting miR-19a level.

关 键 词：糖尿病心肌病 生脉散 氧化应激 miR-19a 过氧化物酶体增殖剂激活受体α 脂肪酸转位酶簇决定因子36 

分 类 号：R285.5[医药卫生—中药学]