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目的探讨α-硫辛酸对糖尿病心肌病大鼠心肌损伤保护作用及其机制。方法 SD大鼠随机分为5组:对照组、糖尿病模型组、α-硫辛酸低、中、高剂量组。以60 mg/kg链脲佐菌素腹腔一次性注射建立大鼠糖尿病模型;α-硫辛酸低、中、高剂量组分别按15、30、60 mg/kg灌胃12周;检测血糖和血清果糖胺,心功能状态;免疫组织化学法和western blot法测定心肌组织基质金属蛋白酶-9(MMP-9)、-2(MMP-2)和金属蛋白酶组织抑制因子-1(TIMP-1)蛋白表达。结果与对照组比较,糖尿病模型组大鼠血糖值/血清果糖胺含量明显升高(P<0.05),心肌组织中MMP-2、MMP-9和TIMP-1蛋白表达及MMP-9/TIMP-1比值明显增加(P<0.05);与糖尿病模型组比较,α-硫辛酸中剂量组血糖[(14.25±3.23)mmol/L]和血清果糖胺[(3.05±0.20)mmol/L]含量明显降低(P<0.05),左室舒张末压[(5.60±0.98)mmHg]明显降低(P<0.05),左心室收缩压[(127.55±5.45)mmHg]明显升高(P<0.05);α-硫辛酸中剂量组MMP-2、MMP-9、TIMP-1蛋白表达分别为62.26、76.78、72.87,明显减少(P<0.05)。结论α-硫辛酸对糖尿病大鼠心肌组织具有保护作用,其机制可能与细胞因子及细胞外基质组成异常有关。
Objective To investigate the protective effect and its mechanism of α-lipoic acid on myocardial injury in diabetic cardiomyopathy rats. Methods SD rats were randomly divided into 5 groups: control group, diabetic model group, α-lipoic acid low, medium and high dose groups. Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (60 mg / kg). The low, medium and high doses of α-lipoic acid were given respectively to stomach at 15, 30 and 60 mg / kg for 12 weeks. Blood glucose and serum Fructosamine, and cardiac function. The expressions of MMP-9, TIMP-1 and TIMP-1 in myocardium were detected by immunohistochemistry and western blot. expression. Results Compared with the control group, the levels of serum glucose and serum fructosamine in diabetic rats were significantly increased (P <0.05). The expressions of MMP-2, MMP-9 and TIMP-1 in myocardium and the expressions of MMP- 1 was significantly increased (P <0.05). Compared with diabetic model group, the levels of [(14.25 ± 3.23) mmol / L] and serum fructosamine [(3.05 ± 0.20) mmol / L] (P <0.05). Left ventricular systolic pressure ([(127.55 ± 5.45) mmHg] was significantly increased (P <0.05); α The protein expressions of MMP-2, MMP-9 and TIMP-1 in the medium dose of lipoic acid were 62.26, 76.78 and 72.87, respectively, which were significantly decreased (P <0.05). Conclusion α-lipoic acid has a protective effect on myocardial tissue of diabetic rats, and its mechanism may be related to abnormal cytokines and extracellular matrix composition.