姜黄素对糖尿病脑病大鼠氧化应激及海马iNOS表达的影响

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目的探讨糖尿病脑病与氧化应激和诱导型一氧化氮合酶(iNOS)的关系,及姜黄素治疗的效果和机制。方法大鼠随机分为正常对照组(CN)、正常姜黄素组(Cur)、糖尿病组(DM)、糖尿病+姜黄素治疗组(DM+Cur),以注射链脲佐菌素建立糖尿病大鼠模型,Cur组和DM+Cur组采用Cur(60mg·kg-1.d-1)灌胃给药。12周后测定海马组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及丙二醛(MDA)、一氧化氮(NO)含量,RT-PCR和免疫组化方法检测海马iNOSmRNA表达水平及iNOS免疫阳性细胞平均光密度值(MOD)值。结果与CN组相比,DM组海马组织SOD和CAT活性明显降低(P<0.01),NO和MDA含量明显增加(P<0.01),海马组织iNOSmRNA及蛋白表达较CN组明显增加(P<0.01);与DM组相比,DM+Cur组SOD和CAT活性明显增加(P<0.01),NO和MDA含量明显降低(P<0.01),海马组织iNOSmRNA及MOD值明显降低(P<0.01)。结论糖尿病脑病与氧化应激水平及海马组织iNOS表达升高相关;姜黄素可能通过抗氧化活性及下调iNOS表达,而对糖尿病脑病起保护作用。 Objective To investigate the relationship between diabetic encephalopathy and oxidative stress and inducible nitric oxide synthase (iNOS) and the effect and mechanism of curcumin treatment. Methods The rats were randomly divided into normal control group (CN), normal curcumin group (DM), diabetes mellitus + curcumin treatment group (DM + Cur) and streptozotocin Model, Cur and DM + Cur groups were administrated with Cur (60mg · kg-1.d-1) intragastrically. The activities of superoxide dismutase (SOD), catalase (CAT) and the content of malondialdehyde (MDA) and nitric oxide (NO) in the hippocampus were measured after 12 weeks. The expression of iNOS mRNA in hippocampus was detected by RT-PCR and immunohistochemistry The expression level and mean optical density (MOD) value of iNOS immunopositive cells. Results Compared with CN group, the activities of SOD and CAT in hippocampus of DM group were significantly decreased (P <0.01) and the levels of NO and MDA were significantly increased (P <0.01). The expression of iNOS mRNA and protein in hippocampus was significantly increased ). Compared with DM group, the activities of SOD and CAT in DM + Cur group were significantly increased (P <0.01), NO and MDA contents were significantly decreased (P <0.01), and hippocampus iNOS mRNA and MOD values ​​were significantly decreased (P <0.01). Conclusions Diabetic encephalopathy is associated with oxidative stress and the increase of iNOS expression in hippocampus. Curcumin may protect against diabetic encephalopathy through its antioxidant activity and down-regulation of iNOS expression.
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