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观察糖康抗氧化应激对实验性糖尿病大鼠视网膜病变的疗效并探讨其作用机制。采用腹腔注射链脲佐菌素(STZ)复制糖尿病模型并随机分为正常对照组、模型组、糖康高、中和低剂量组和达纳康组,每日灌胃,定期检测大鼠体重和非空腹血糖;第12周末,消化铺片法观察视网膜微血管病理和形态学改变;化学比色法检测各组大鼠血清及视网膜组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。与正常组比较,模型组血清及视网膜SOD活性明显降低(P<0.01),MDA含量明显升高(P<0.01),无细胞毛细血管条索数明显升高,约为正常组的5.33倍(P<0.01);与模型组比较,各治疗组均可提高血清及视网膜SOD活性,降低MDA含量,且以糖康高剂量组最为显著(P<0.01),无细胞毛细血管条索数明显降低(P<0.01)。糖康可显著降低糖尿病大鼠的氧化应激水平,提高糖尿病大鼠血清及视网膜的抗氧化能力。
To observe the effect of Kangkang anti-oxidative stress on retinopathy in experimental diabetic rats and to explore its mechanism. The model of diabetes mellitus was established by intraperitoneal injection of streptozotocin (STZ) and randomly divided into normal control group, model group, high glucose, medium and low dose groups and Danan Kang group. And non-fasting blood glucose (FBG). At the end of the 12th week, the pathological and morphological changes of retinal microvessels were observed by digestion-spreading method. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in the serum and the retina were detected by chemical colorimetry )content. Compared with normal group, the activity of SOD in serum and retina of model group decreased significantly (P <0.01), MDA content increased significantly (P <0.01), and the number of acellular capillaries significantly increased, which was 5.33 times of that of normal group P <0.01). Compared with the model group, the activity of SOD in serum and retina were increased and the content of MDA was decreased in all treatment groups, especially in the high dose of Tangkang group (P <0.01), and the number of acellular capillaries was significantly decreased (P <0.01). Tangkang can significantly reduce the oxidative stress in diabetic rats and improve the antioxidant capacity of serum and retina in diabetic rats.