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积雪草酸对糖尿病大鼠肾脏Nrf2-ARE信号通路的影响 被引量:4

Effect of asiatic acid on Nrf2-ARE signaling pathway in the kidney of diabetic rats
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摘要 目的探讨积雪草酸(AA)对糖尿病大鼠肾脏氧化应激及核因子NF-E2相关因子(Nrf2)-抗氧化反应元件(ARE)信号通路的影响。方法 18只雄性SD大鼠随机均分为糖尿病模型组(DM组)、AA 60mg.kg-1.d-1干预组(AA组)和正常对照组(NC组)。干预8周后,检测各组血糖、肾脏指数(KI)、血尿素氮(BUN)、血清肌酐(SCr)、尿白蛋白排泄率(UAER)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,光镜下观察肾脏的病理形态改变,Western blot法检测Nrf-2、血红素氧合酶1(HO-1)蛋白表达。结果与NC组相比,DM组肾脏病理形态改变明显,血糖、KI、BUN、SCr及UAER、MDA和Nrf-2均明显增加(P<0.05),SOD活性、HO-1蛋白表达降低(P<0.05);而AA组能明显改善上述指标的变化(P<0.05)。结论 AA可能通过激活Nrf2-ARE信号通路发挥对糖尿病大鼠肾脏的保护作用。 Objective To investigate the effect of asiatic acid(AA) on renal oxidative stress and Nrf2-ARE signaling pathway in diabetic rats. Methods Eighteen male SD rats were randomized into three groups of DM(diabetes mellitus model), AA(treated with AA 60 mg · kg-1 d-1) and NC (normal control). After intervened for 8 weeks, the levels of blood glucose, kidney index(KI), blood urea nitrogen(BUN), serum creatinine(SCr), urine albumin excretion rate(UAER), the content of malondialdehyde(MDA) and the activity of superoxide dismutase(SOD) in the renal cortex were detected. The pathologic changes of kidney were observed under optics microscope. And the protein expressions of Nrf-2 and HO-1 were examined by Western blot. Results Compared with group NC, the pathologic morphology of the kidney was obviously changed, the levels of blood glucose and KI, BUN, SCr, UEAR, content of MDA and protein expression of Nrf-2 were significantly increased (P〈0. 05) ,while the activity of SOD and protein expression of HO-1 were decreased(P〈0. 05) in group DM,which were all remarkably improved in group AA(P〈0. 05). Conclusion AA may protect the kidney of diabetic rats via activating Nrf2-ARE signaling pathway.
出处 《江苏医药》 CAS 北大核心 2013年第12期1381-1383,F0003,共4页 Jiangsu Medical Journal
基金 江苏省卫生厅面上项目(H200830) 镇江市科技支撑社会发展项目(SH2010018) 镇江市科技支撑社会发展项目(SH2011032)
关键词 糖尿病肾病 氧化应激 积雪草酸 核因子NF-E2相关因子 血红素氧合酶1 Diabetic nephropathy Oxidative stress Asiatic acid Nuclear tactor erythroid-2-related factor-2 ~ Heme oxygenase-1
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参考文献6

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共引文献27

同被引文献45

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