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目的:探讨归芪方对糖尿病(DM)大鼠心肌病变的保护作用及其机制。方法:将21只SD大鼠腹腔注射链脲佐菌素(STZ)建立DM模型,按随机数字表法分为DM模型组(D组)、贝那普利治疗组(B组)、归芪方治疗组(G组)。另7只作为空白正常对照组(N组)。G组给予归芪方4.5 g/(kg.d),B组给予贝那普利片10 mg/(kg.d),D组及N组注射等体积的柠檬酸缓冲液。各组大鼠于第8周末处死,测定各组血糖、血脂、心脏重、体重的改变;观察心肌组织Ⅰ、Ⅲ胶原及血管紧张素Ⅱ(AngⅡ)的表达,荧光定量PCR法检测心肌转化生长因子-β1(TGF-β1)及结缔组织生长因子-β1(CTGFβ-1)mRNA的表达。结果:归芪方改善了血糖、血脂异常及抑制Ⅰ、Ⅲ胶原、血管紧张素Ⅱ(AngⅡ)、TGFβ-1、CTGF-β1mRNA的高表达(P<0.05),且在抑制心肌TGF-β1、CTGFβ-1mRNA方面的表达归芪方优于贝那普利组(P<0.01,P<0.05)。结论:归芪方可调节糖尿病大鼠受损的糖、脂代谢异常,抑制心肌TGFβ-1、CTGFβ-1mRNA的表达,延缓糖尿病心血管并发症的进展。
Objective: To investigate the protective effect of Guiqi decoction on myocardial lesions in diabetic rats and its mechanism. METHODS: A total of 21 SD rats were intraperitoneally injected with streptozotocin (STZ) to establish a DM model. According to the random number table method, they were divided into DM model group (D group), benazepril treatment group (B group), and indwelling group. Square treatment group (group G). The other 7 were used as blank control group (N group). G group was given 4.5 g/(kg.d) of guinea pig, Benazepril group was given 10 mg/(kg.d) in group B, and group C and group C were injected with equal volumes of citric acid buffer. Rats in each group were sacrificed at the end of the 8th week. Blood glucose, blood lipids, heart weight, and body weight were measured. The expression of collagen I and III and AngII in myocardial tissue were observed. Fluorescent quantitative PCR was used to detect myocardial growth. Expression of factor-β1 (TGF-β1) and connective tissue growth factor-β1 (CTGFβ-1) mRNA. RESULTS: Guiqifang improved blood glucose and dyslipidemia and inhibited the high expression of collagen I, III, angiotensin II (AngII), TGFβ-1 and CTGF-β1 mRNA (P<0.05), and inhibited myocardial TGF-β1. The expression of CTGFβ-1 mRNA was better than that of benazepril group (P<0.01, P<0.05). Conclusion: Guiqi recipe can regulate abnormal glucose and lipid metabolism in diabetic rats, inhibit the expression of myocardial TGFβ-1 and CTGFβ-1 mRNA and delay the progression of diabetic cardiovascular complications.