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目的 :探讨黄芪对糖尿病大鼠心肌的保护作用机制。方法 :用雌性 4周龄wistar大鼠 5 2只 ,高糖高脂饮食喂养 4周造成胰岛素抵抗后 ,随机选其中 7只腹腔注射枸橼酸钠缓冲液为对照组 1;其余用链脲佐菌素 (STZ)腹腔注射诱发糖尿病 ,2 0周后成功复制糖尿病心肌病 ,通过颈动脉插管将等容舒张期左室内压下降的最大速率 ( dp/dtmax)≤ 70 0mmHg的糖尿病大鼠 ( 2 4只 )分组 :7只用双蒸水腹腔注射 ,为对照组 2 ;8只通过腹腔注射AT2 激动剂 (CGP 4 2 112A) ,为实验组 1;9只腹腔注射黄芪注射液 ,为实验组 2。以上注射每天一次连续 4周。称心脏重量 ,通过凋亡试剂盒检测心肌细胞凋亡指数 ,WesternBlot,免疫组化染色法检测心肌细胞上AT2 和Bcl 2蛋白质量。结果 :实验组 1和 2、对照组 2 dp/dtmax ,显著低于对照组 1(P <0 .0 1) ;三组糖尿病大鼠心肌细胞凋亡指数、AT2 的蛋白质表达量及心脏重量均显著高于对照组 1(P <0 .0 1) ;实验组 1、2心肌凋亡指数、AT2 的蛋白质表达量分别显著高于、显著低于对照组 2 (P <0 .0 1) ;实验组 1心肌凋亡指数、AT2 的蛋白质表达量及心脏重量测定分别显著高于实验组 2 (P <0 .0 1) ;Bcl 2变化与AT2 变化相反。结论 :AT2 高表达促进糖尿病大鼠心肌细胞的凋亡 ,是糖尿病心肌病的重要促?
Objective: To explore the protective mechanism of Astragalus membranaceus in diabetic rats. Methods: A total of 52 female 4-week-old wistar rats were fed with a high-sugar and high-fat diet for 4 weeks to induce insulin resistance. Seven of them were randomly selected as the control group 1 with intraperitoneal injection of sodium citrate buffer; Intraperitoneal injection of STZ induces diabetes mellitus. Diabetic cardiomyopathy was successfully replicated after 20 weeks. Diabetic rats (dp/dtmax) with a maximum rate of diastolic left intraventricular pressure (dp/dtmax) ≤ 70 mmHg were intubated through the carotid artery. 2) 4 groups: 7 mice were given intraperitoneal injections of double distilled water, which were control group 2; 8 rats were given intraperitoneal injection of AT2 agonist (CGP 4 2 112A) as experimental group 1; 9 rats were given intraperitoneal injection of Huangqi injection as experiment Group 2. The above injections are repeated once a day for 4 weeks. The cardiac weight was measured by apoptotic kit to detect myocardial cell apoptosis index. Western Blot and immunohistochemical staining were used to detect the AT2 and Bcl 2 protein content on cardiomyocytes. RESULTS: The 2 dp/dtmax of the experimental group 1 and 2 was significantly lower than that of the control group 1 (P < 0.01); the cardiomyocyte apoptosis index, AT2 protein expression and heart weight were all in the three groups of diabetic rats. Significantly higher than control group 1 (P <0. 01); myocardial apoptosis index and AT2 protein expression in experimental groups 1 and 2 were significantly higher than those in control group 2 (P <0.01); The experimental group 1 myocardial apoptosis index, AT2 protein expression and cardiac weight were significantly higher than the experimental group 2 (P <0. 01); Bcl 2 changes and AT2 changes in the opposite. Conclusion : High expression of AT2 promotes apoptosis of cardiomyocytes in diabetic rats and is an important promotion of diabetic cardiomyopathy.