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Primary study of Astragalus polysaccharides in inhibiting myocardial oxidative stress of diabetes mellitus |
CHEN Wei1▲ JU Jing1 WANG Hao2 WANG Liying2 YANG Yehong3 YE Hongying3 LI Yiming3 ZHANG Yu1▲ |
1.Department of Geriatrics, Huashan Hospital, Fudan University, Shanghai 200040, China;
2.Experimental Teaching Center of Basic Medicine, Fudan University, Shanghai 200032, China;
3.Department of Endocrinology, Huashan Hospital, Fudan University, Shanghai 200040, China |
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Abstract Objective To investigate the effect of Astragalus polysaccharides for myocardial oxidative stress of diabetes mellitus. Methods Sixteen male healthy transgenic SOD2+/-KO mice aged 6-8 weeks old (C57BL/6J) were randomly divided into transgenic group and Astragalus polysaccharides transgenic group by random number table method (n = 8). The 24 normal control mice were divided into control group, diabetes mellitus group and Astragalus polysaccharides diabetes mellitus group (n = 8). Single intraperitoneal injection of Streptozotocin was utilized to establish mice model with diabetes mellitus in diabetes mellitus group and Astragalus polysaccharides diabetes mellitus group, after the diabetes mellitus model was made successfully, the mice in Astragalus polysaccharides diabetes mellitus group and Astragalus polysaccharides transgenic group were treated with Astragalus Polysaccharides Injection for 16 weeks, and the other groups were given equal amount of normal saline. Echocardiography was used to detect cardiac function, HE staining was used to observe the structure of myocardial tissue, ultrasonic electron microscopy was used to observe the myocardial ultrastructure, immunohistochemistry was used to detect the proliferative activity of cardiomyocytes, TUNEL method was used to detect apoptosis of cardiomyocytes; fluorescent quantitative assay was used to detect the contents of myocardial reactive oxygen species (ROS), Western blot was used to detect the contents of myocardial SOD2 protein, calbiochem SOD assay kit Ⅱ was used to detect the activity of myocardial SOD2. Results Compared with the control group, LVSP and ±LVdp/dt in diabetes mellitus group and transgenic group were decreased, and LVEDP was increased, myocardial tissue and ultrastructure were seriously damaged, the degree of cells apoptosis and necrosis was increased, and the activity of SOD2 was significantly inhibited. However, the indices above in the Astragalus polysaccharides were all signifcantly improved (P < 0.05). Conclusion Astragalus polysaccharides can inhibit the myocardial oxidative stress injury of diabetes mellitus.
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