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目的:探讨α-硫辛酸对STZ所致Ⅱ型糖尿病大鼠心肌损伤的保护作用及其机制。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。后4组采用小剂量链尿佐菌素(Streptozocin,STZ)30 mg.kg-1腹腔注射,建立Ⅱ型糖尿病模型。α-硫辛酸低、中、高剂量组分别按15,30,60 mg.kg-1灌胃12周。检测血糖和血脂,心功能状态;HE染色观察大鼠心肌形态变化;免疫组织化学法和Western Blot法测定心肌组织核因子-κB(NF-κB)、细胞间黏附因子-1(ICAM-1)和单核趋化蛋白-1(MCP-1)蛋白表达。结果:与对照组比较,糖尿病组大鼠血糖及三酰甘油(TG)、胆固醇(TC)、低密度脂蛋白(LDL)明显增高(P<0.01),高密度脂蛋白(HDL)明显降低(P<0.01),心肌组织中NF-κB、ICAM-1、MCP-1蛋白表达显著增加(P<0.05);与糖尿病组比较,α-硫辛酸30 mg.kg-1血糖及TG、TC、LDL明显降低(P<0.05),HDL显著提高(P<0.05);LVEDP[(5.6±1.0)mmHg]明显降低(P<0.05),LVSP[(127.6±5.4)mmHg]明显升高(P<0.05);α-硫辛酸30 mg.kg-1组NF-κB、ICAM-1、MCP-1蛋白表达明显减少(P<0.05)。结论:α-硫辛酸对Ⅱ型糖尿病大鼠心肌有保护作用,其机制可能与降糖、降脂、抑制炎症因子有关。
Objective: To investigate the protective effect of α-lipoic acid on myocardial injury induced by STZ in type 2 diabetic rats and its mechanism. Methods: SD rats were randomly divided into 5 groups: control group, diabetic model group, α-lipoic acid low, medium and high dose groups. The latter four groups were given type Ⅱ diabetes mellitus by intraperitoneal injection of low dose streptozocin (STZ) 30 mg.kg-1. α-lipoic acid low, medium and high dose groups were 15,30,60 mg.kg-1 gavage for 12 weeks. The blood glucose, blood lipid and cardiac function were detected. The morphological changes of myocardium were observed by HE staining. The expressions of nuclear factor-κB, ICAM-1 and NF-κB in myocardium were detected by immunohistochemistry and Western Blot. And monocyte chemotactic protein-1 (MCP-1) protein expression. Results: Compared with the control group, the levels of blood glucose, triglyceride (TG), cholesterol (TC) and low density lipoprotein (LDL) and the content of high density lipoprotein (HDL) (P <0.01). The expression of NF-κB, ICAM-1 and MCP-1 in myocardium were significantly increased (P <0.05). Compared with diabetic group, (P <0.05); LVEDP [(5.6 ± 1.0) mmHg] was significantly lower (P <0.05) and LVSP [(127.6 ± 5.4) mmHg] 0.05). The protein expressions of NF-κB, ICAM-1 and MCP-1 in α-lipoic acid 30 mg · kg-1 group were significantly decreased (P <0.05). Conclusion: α-lipoic acid has a protective effect on myocardium in type 2 diabetic rats. The mechanism may be related to hypoglycemic, lipid-lowering, and inflammatory cytokines.