参芪复方对自发性糖尿病大鼠血管内皮保护的作用机制

目的:观察参芪复方对自发性糖尿病(GK)大鼠2型糖尿病(T2DM)大血管病变血管内皮保护的影响。方法:将血糖11.1 mmol/L以上的44只大鼠随机分为模型组、雷米普利组、参芪复方低剂量组、参芪复方高剂量组。4组GK大鼠腹腔注射N-硝基-L-精氨酸甲酯(L-NAME)造模,高脂饮食14天。正常对照组给生理盐水。造模后给受试药物28天。用ELISA法测细胞间黏附分子-1(ICAM-1),放免法测血浆内皮素-1(ET-1),比色法测一氧化氮合酶(NOS),硝酸还原酶法测一氧化氮(NO),实时定量PCR法测胸主动脉ICAM-1mRNA表达。结果:参芪复方组的血清NO、NOS较模型组明显升高,ET-1明显降低(P<0.01),胸主动脉I-CAM-1 mRNA的表达显著低于模型组(P<0.01),血清NO与血浆ET-1的相关系数r=-0.90,P<0.01。结论:参芪复方能下调GK大鼠内皮细胞损伤的ICAM-1 mRNA的表达,抑制ICAM-1的生成,调节NO-ET系统,可能是参芪复方治疗T2MD大血管病变的机制之一。

Mechanism of ShenQi compound recipe on preserving vessel endothelium in GK rats

Objective: To explore the mechanism of ShenQi compound recipe on preserving vessel endothelium with type 2 diabetes mellitus(T2DM) macroangiopathy in GK rats.Methods: GK rats were randomly divided into Ramipril group,ShenQi compound recipe low dosage group,ShenQi compound recipe high dosage group and Wistar control group.Each group was administrated correspondent substance respectively for 28 days after intra-peritoneal injection of L-NAME and administration of high fat diet for 2 weeks except Wistar control group.To determine ICAM1 by ELISA,ET-1 by radioimmunassay,NOS by chemical shade selection,NO by nitrate reductase method,mRNA expression of ICAM-1 in aorta by real time RT-PCR. Results: Compared with model group,the contents of NO,NOS increased,the ET1 and the expression of thoracic aorta ICAM-1mRNA decreased remarkably in ShenQi compound recipe group(P<0.01),serum NO correlated negatively with blood plasm ET-1(r=-0.90,P<0.01).Conclusion: ShenQi compound recipe can decrease the expression of thoracic aorta ICAM-1mRNA,inhibit the production of ICAM-1,regulate NO-ET system in GK rats.This may be one of the mechanisms of ShenQi compound recipe on treating T2DM macroangiopathy.