EGCG调节PI3KAKT信号通路保护肾功能机制研究.docVIP

EGCG调节PI3KAKT信号通路保护肾功能机制研究.doc

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EGCG调节PI3KAKT信号通路保护肾功能机制研究

EGCG调节PI3KAKT信号通路保护肾功能机制研究   [摘要] 目的 探?表没食子儿茶素没食子酸酯(EGCG)对糖尿病肾病(DN)大鼠的保护作用。 方法 48只雄性SD大鼠随机分为三组,每组16只。Control组给予正常饮食,DN组采用高脂饮食联合链脲佐菌素(STZ)50 mg/kg腹腔注射建立DN模型,EGCG组给予EGCG 50 mg/kg每天灌胃治疗,同DN组大鼠予以相同体积生理盐水。分别在6周和12周处死大鼠各半,收集血清和肾脏,采用ELISA、RT-qPCR和Western blot等方法检测相关因子。 结果 与Control组比较,DN组血清中肾功能指标、炎症因子以及血脂水平升高(P 0.05),EGCG治疗6周后,与DN组比较,EGCG组上述指标下降(P 0.05);与Control组比较,DN组大鼠血清中抗氧化因子含量降低(P 0.05),治疗6周后,与DN组比较,EGCG组上述指标升高(P 0.05);与Control组比较,DN组大鼠肾脏组织中p-PI3K和p-AKT的蛋白表达下调(P 0.05),治疗6周后,与DN组比较,EGCG组p-PI3K和p-AKT的蛋白表达水平上调(P 0.05),治疗12周后上述指标进一步改善。结论 EGCG可通过减少体内炎症反应与脂质沉积,改善肾功能、增加抗氧化能力以及抗细胞凋亡等途径治疗DN大鼠肾脏损伤。   [关键词] 表没食子儿茶素没食子酸酯;糖尿病肾病;磷脂酰肌醇-3-激酶;丝苏氨酸蛋白激酶   [中图分类号] R587 [文献标识码] A [文章编号] 1673-7210(2016)12(c)-0031-05   [Abstract] Objective To explore the protective effect of EGCG on diabetic DN rats. Methods 48 male SD rats were divided into 3 groups respectively, each group had 16 rats. Rats in the control group were given normal diet, while rats in the other groups were fed with a high-fat diet accompanied with intraperitoneal injection of STZ (50 mg/kg) to establish DN model. Then the rats in the EGCG group were given EGCG (50 mg/kg) by lavage every day, at the same time the DN group were given the same volume of saline. Half of the rats in each group were killed at 6 or 12 weeks respectively, the serum and kidney tissues were collected. The related factors were determined by ELISA, RT-qPCR and Western blot. Results Compared with the control group, the concentrations of indicaters of renal function, inflammatory and lipids in the DN group were increased (P 0.05), after EGCG treatment for 6 weeks, compared with the DN group, these indexes in the EGCG group were decreased (P 0.05). Compared with the control group, the contents of anti-oxdators in the DN group were reduced (P 0.05), after EGCG treatment for 6 weeks, compared with the DN group, these parameters in the EGCG group were elevated (P 0.05). Compared with the control group, the protein expression levels of p-PI3K and

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