论文部分内容阅读
目的观察二甲双胍(MET)对T2DM模型SD大鼠肾组织蛋白激酶C-β(PKC-β)mRNA和蛋白表达的影响,探讨MET对糖尿病肾脏疾病(DKD)肾损害的保护机制。方法高脂饲料喂养合并从腹腔注射小剂量STZ建立T2DM大鼠模型。随机分为正常对照组(NC,n=10)及模型组(DM组,n=32)。27只大鼠造模成功后再将其随机分成二甲双胍治疗组(MET,n=8)、格列本脲治疗组(GLY,n=9)及糖尿病对照组(T2DM,n=10)。给药8周后,观察各组HbA_1c、FBG、BUN尿白蛋白排泄和基底膜厚度(GBMT)情况;同时检测肾小球PKC-β蛋白表达和肾组织PKC-β_(mRNA)表达情况。结果 8周末,与NC组比较,T2DM组FBG[(4.45±1.07)vs(15.6±1.56)mmol/L]和HbA_1c[(4.13±0.89)%vs(12.41±0.61)%]升高(P<0.05),PKC-β_(IOD)[(22.24±2.39)vs(42.00±4.90)]和PKC-β_(mRNA)[(1.00±0.04)vs(2.16±0.13)]升高(P<0.05);与T2DM组比较,MET组PKC-β_(IOD)[(42.00±4.90)vs(27.32±1.71)]和PKC-β_(mRNA)[(2.16±0.13)vs(1.11±0.02)]降低(P<0.05);与GLY组比较,MET组PKC-β_(IOD)[(30.73±1.95)vs(27.32±1.71)]和PKC-β_(mRNA)[(1.75±0.02)vs(1.11±0.02)]降低(P<0.05)。结论 MET可减轻PKC-β在T2DM大鼠肾组织的高表达,该作用可能是其肾脏保护机制之一。
Objective To observe the effect of metformin (MET) on the protein and protein expression of PKC-β in the kidney of SD rats with T2DM and to explore the protective mechanism of MET on renal damage in diabetic nephropathy (DKD). Methods High fat diet fed combined with low dose STZ injected intraperitoneally to establish T2DM rat model. Randomly divided into normal control group (NC, n = 10) and model group (DM group, n = 32). Twenty-seven rats were randomly divided into metformin-treated group (MET, n = 8), glibenclamide-treated group (GLY, n = 9) and diabetic control group (n = 10). Eight weeks after the administration, urinary albumin excretion and basement membrane thickness (GBMT) of HbA 1c, FBG and BUN in each group were observed. PKC-β protein expression in glomerulus and PKC-β_ (mRNA) expression in renal tissue were detected. Results Compared with NC group, FBG [(4.45 ± 1.07) vs (15.6 ± 1.56) mmol / L] and HbA1c [(4.13 ± 0.89)% vs (12.41 ± 0.61)%] (P <0.05), PKC-β_ (IOD) [(22.24 ± 2.39) vs (42.00 ± 4.90)] and PKC-β_ (mRNA [1.00 ± 0.04 vs 2.16 ± 0.13] Compared with T2DM group, the levels of PKC-β_ (IOD) [(42.00 ± 4.90) vs (27.32 ± 1.71) and PKC-β_ (mRNA) in MET group [(2.16 ± 0.13 vs 1.11 ± 0.02) 0.05). Compared with GLY group, the levels of PKC-β_ (IOD) [(30.73 ± 1.95) vs (27.32 ± 1.71)] and PKC-β_ (mRNA [1.75 ± 0.02 vs 1.11 ± 0.02] (P <0.05). Conclusion MET can alleviate the high expression of PKC-β in the kidney of T2DM rats, which may be one of the mechanisms of renal protection.