清润方对糖尿病大鼠肝脏PI_3K/AKT/mTOR信号的影响

Effecf of Qingrunfang on Signal Pathway of PI_3K/AKT/mTOR in Liver of Diabetic Rats

目的研究清润方对2型糖尿病胰岛素抵抗大鼠PI_3K/AKT/mTOR信号通路的影响。方法采用脂肪乳灌胃和腹腔注射链脲佐菌素(streptozotocin, STZ)建立2型糖尿病胰岛素抵抗模型。将大鼠随机分成空白对照组、模型组、清润方大剂量组[11.2g/(kg·d)]、清润方中剂量组[5.6g/(kg·d)]、清润方小剂量组[2.8g/(kg·d)]、二甲双胍组[250mg/(kg·d)]。各组均灌胃给药。每天1次,连续8周。干预后检测血清中血清总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、低密度脂蛋白(low density lipoprotein,LDL-C)和高密度脂蛋白(high density lipoprotein,HDL-C),检测肝组织中p-AKT、p-PTEN及p70S6K的mRNA以及蛋白表达水平。结果与模型组比较,清润方大剂量组和二甲双胍组的TC、TG和LDL-C降低,HDL-C升高(P<0.05)。清润方大剂量组的AKT和PTEN的mRNA表达升高(P<0.05),p70S6K的mRNA表达下降(P<0.05),与模型组比较,清润方大剂量组的p-AKT和p-PTEN的蛋白表达升高(P<0.05),p-p70S6K的蛋白表达下降(P<0.05)。结论清润方可能通过PI_3K/AKT/mTOR信号通路来改善胰岛素抵抗。

Objective To study the effect of Qingrunfang on signal pathway of PI3 K/AKT/mTOR of rat with diabetes mellitus. Methods The rats with diabetes mellitus were induced by intraperitoneal injection of streptozotocin and feeding with fat milk for 30 days. Rats with diabetes were randomly divided into five groups,Qingrunfang high dosage groups,Qingrunfang middle dosage groups,Qingrunfang low dosage groups,metformin group and model group,other normal rats were made as control group.After 8 weeks,TC ,TG,LDL-C and HDL-C were measured,qRT -PCR way used to observe mRNA expression of AKT,PTEN and p70S6K.Western blot test way used to observe protein expression of p-AKT,p-PTEN and p-p70S6K.Results Compared with the model group,the levels of TC,TG and LDL-C were decreased in the Qingrunfang high dosage groups (P<0.05 ).The levels of HDL-C were increased in the Qingrunfang high dosage groups (P<0.05).The mRNA expression of AKT and PTEN were increased in qingrunfang high dosage groups (P <0.05 ).The mRNA expression of p70S6K were decreased in the high dosage groups (P<0.05).The protein expression of p -AKT and p-PTEN were increased in qingrunfang high dosage groups (P<0.05).The protein expression of p-p70S6K were decreased in the high dosage groups (P <0.05).Conclusion Qingrunfang may improve the insulin resistance and lipid metabolism by PI3K/AKT/mTOR signal pathway.