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目的研究维生素D是否通过抑制氧化应激在糖尿病肾病(DN)中产生保护作用。方法应用链脲佐菌素(STZ)腹腔注射诱导糖尿病大鼠模型,经过两个月持续喂养诱导DN模型。将大鼠随机分为三组,糖尿病肾病骨化三醇干预组(DNR组)予骨化三醇0.2μg·kg~(-1)·d~(-1)灌胃,正常对照组(NC组)和DN组仅给予等容量花生油,均灌胃一个月。检测给药前后大鼠体重、随机血糖、血脂、血清丙二醛及总超氧化物歧化酶(T-SOD)、总抗氧化能力(T-AOC)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)水平等。电镜观察大鼠肾脏超微结构改变,real-time PCR检测大鼠肾脏谷胱甘肽过氧化物酶1(GPX1)、超氧化物歧化酶1和2(SOD1、SOD2)mRNA表达水平。结果与NC组比较,DN组和DNR组大鼠体重降低,血糖、三酰甘油水平升高(P<0.05或P<0.01)。DN组肾重-体重比和尿微量白蛋白-肌酐比值(UA/Cr)明显高于NC组(P<0.01),DNR组肾重-体重比和UA/Cr均低于DN组(P<0.05或P<0.01)。DN组血清丙二醛水平高于NC组,T-SOD、T-AOC、CAT、GSH-PX活性及肾脏GPX1、SOD1、SOD2 mRNA水平均低于NC组(P<0.01),肾脏超微结构出现明显异常。DNR组血清丙二醛水平低于DN组,T-SOD、T-AOC、CAT、GSH-PX活性及肾脏GPX1、SOD1、SOD2 mRNA水平均高于DN组(P<0.05或P<0.01),肾脏超微结构异常明显改善。结论维生素D可能通过增加肾脏的抗氧化能力减轻DN大鼠的氧化应激,从而发挥其对DN的保护作用。
Objective To investigate whether vitamin D can protect diabetic nephropathy (DN) by inhibiting oxidative stress. Methods Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ), and were induced by continuous feeding for two months. The rats were randomly divided into three groups. The diabetic nephropathy calcitriol intervention group (DNR group) received calcitriol 0.2 μg · kg -1 d -1, and the normal control group (NC Group) and DN group were given only the capacity of peanut oil, were gavage for a month. The body weight, blood glucose, serum MDA, T-SOD, T-AOC, CAT, Glycopeptide peroxidase (GSH-PX) levels and so on. The changes of renal ultrastructure in rats were observed by electron microscope. The expression of glutathione peroxidase 1 (GPX1), superoxide dismutase 1 and 2 (SOD1, SOD2) mRNA in kidney of rats were detected by real-time PCR. Results Compared with NC group, the body weight of DN group and DNR group decreased, blood glucose and triglyceride levels increased (P <0.05 or P <0.01). The ratio of renal weight to body weight and urinary albumin to creatinine (UA / Cr) in DN group was significantly higher than that in NC group (P <0.01), while the ratio of renal weight to body weight and UA / Cr in DNR group were lower than those in DN group (P < 0.05 or P <0.01). The serum malondialdehyde level in DN group was higher than that in NC group. The activities of T-SOD, T-AOC, CAT, GSH-PX and the levels of GPX1, SOD1 and SOD2 in DN group were lower than those in NC group Significant abnormalities occurred. The serum malondialdehyde level in DNR group was lower than that in DN group. The activities of T-SOD, T-AOC, CAT, GSH-PX and the levels of GPX1, SOD1 and SOD2 mRNA in DNR were higher than those in DN (P <0.05 or P <0.01) Abnormal renal ultrastructure was significantly improved. Conclusion Vitamin D may reduce the oxidative stress in DN rats by increasing the antioxidant capacity of kidney and thus exert its protective effect on DN.