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目的:探讨葛根素对实验性糖尿病大鼠胰腺线粒体保护作用的机制。方法:30只Wistar大鼠随机分为正常对照组、糖尿病组和治疗组。采用四氧嘧啶腹腔注射复制糖尿病动物模型。葛根素注射液治疗8周后,观测胰腺线粒体中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)及一氧化氮合酶(NOS)活力;测定胰腺线粒体丙二醛(MDA)及一氧化氮(NO)含量。结果:葛根素治疗组胰腺线粒体SOD、GSH-Px活力较糖尿病组均有显著升高(P<0.01或P<0.05),而NOS活力、MDA及NO含量明显降低(P<0.01或P<0.05)。结论:葛根素对糖尿病大鼠胰腺有保护作用。其机制可能是:清除自由基,减少脂质过氧化物的生成;降低线粒体NOS活力,从而减轻NO所致的损伤。
Objective: To investigate the protective mechanism of puerarin on pancreatic mitochondria in experimental diabetic rats. Methods: Thirty Wistar rats were randomly divided into normal control group, diabetic group and treatment group. Alloxan was injected intraperitoneally to replicate diabetic animal models. After eight weeks of puerarin injection, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and nitric oxide synthase (NOS) in the mitochondria of the pancreas were observed; Aldehyde (MDA) and nitric oxide (NO) content. Results: The activity of SOD and GSH-Px in the mitochondria of the puerarin group was significantly higher than that of the diabetic group (P<0.01 or P<0.05), but the NOS activity, MDA and NO were significantly decreased (P<0.01 or P<0.05). ). Conclusion: Puerarin can protect pancreas of diabetic rats. The mechanism may be: scavenging free radicals, reducing the production of lipid peroxides; reducing mitochondrial NOS activity, thereby reducing NO-induced damage.