|本期目录/Table of Contents|

[1]姚晶瑞,姜埃利,王立华,等.雷公藤甲素上调PRDX2抑制2型糖尿病肾病的氧化应激状态[J].天津医科大学学报,2019,25(05):466-470.
 YAO Jing-rui,JIANG Ai-li,WANG Li-hua,et al.Inhibition of Triptolide on oxidase stress via PRDX2 expression in diabetic nephropathy[J].Journal of Tianjin Medical University,2019,25(05):466-470.
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雷公藤甲素上调PRDX2抑制2型糖尿病肾病的氧化应激状态(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
25
期数:
2019年05期
页码:
466-470
栏目:
基础医学
出版日期:
2019-09-20

文章信息/Info

Title:
Inhibition of Triptolide on oxidase stress via PRDX2 expression in diabetic nephropathy
文章编号:
1006-8147(2019)05-0466-05
作者:
姚晶瑞12姜埃利1王立华1魏 芳1陈海燕1于海波1孟 甲1
(1.天津医科大学第二医院肾脏病血液净化科,天津300211;2. 天津市海河医院肾内科,天津300350)
Author(s):
YAO Jing-rui12 JIANG Ai-li1 WANG Li-hua1 WEI Fang1 CHEN Hai-yan1 YU Hai-bo1 MENG Jia1
(1.Department of Renal Disease and Blood Purification, The Second Hospital, Tianjin Medical University, Tianjin 300211,China;2.Department of Nephrology, Haihe Hospital, Tianjin 300350,China)
关键词:
PRDX2雷公藤甲素糖尿病肾病人肾小球系膜细胞
Keywords:
PRDX2 triptolidediabetic nephropathyhuman mesangialcells
分类号:
R587.1
DOI:
-
文献标志码:
A
摘要:
目的:通过观察雷公藤甲素对2型糖尿病肾病小鼠肾脏和人肾小球系膜细胞氧化应激的影响,探讨雷公藤甲素改善2型糖尿病肾病的分子机制。方法:体内实验分3组:C57小鼠对照组、KK-Ay小鼠模型组和KK-Ay小鼠加用雷公藤甲素干预组。雷公藤甲素200 μg/(kg·d)灌胃12周后取肾脏组织进行HE染色;体外实验采用人肾小球系膜细胞为研究对象,分为正常糖组、高糖刺激模型组和雷公藤甲素干预组3组。分别用含有5.5 mmol/L(培养基组成)的D-葡萄糖、30 mmol/L的D-葡萄糖、及30 mmol/L的D-葡萄糖加10 μg/L的雷公藤甲素培养24 h。采用ELISA法检测小鼠肾脏和人肾小球系膜细胞中SOD活性和MDA含量。Western blot方法检测各组小鼠肾脏和人肾小球系膜细胞中PRDX2的蛋白表达量。结果:体内外实验结果均显示,与相应对照组相比,2型糖尿病肾病小鼠模型组肾脏和人肾小球系膜细胞高糖刺激模型组细胞中SOD活性明显下降,MDA含量明显增加,PRDX2蛋白表达水平明显降低(P<0.05);雷公藤甲素干预组较模型组SOD活性明显升高,MDA含量明显减少,同时PRDX2蛋白表达水平明显增加(P<0.05)。结论:雷公藤甲素可以通过上调PRDX2抑制2型糖尿病肾病肾脏氧化应激状态。
Abstract:
Objective: To study the effect of Triptolide on oxidase stress in kidneys of mice with diabetic nephropathy and human mesangial cells. Methods: Three groups of mice were used in the in vivo experiments. The three groups were C57 mice controls, KK-Ay mice models, and test group of KK-Ay mice models by triptolide treatment. At the end of treatment, histopathological examination was done to examine the glomerular injury. The human mesangial cells were used in the in vitro experiments and were divided into three groups, the control group, the high glucose model group, and test group of high glucose by triptolide treatment. The MDA contents and the SOD activities in different groups were detected by ELISA. The PRDX2 protein levels were valued by Western blot. Results: The decreased SOD activities, the increased MDA contents, and the decreased PRDX2 protein levels were determined in kidney of KK-Ay mice models and the high glucose model group compared with the corresponding control groups(P<0.05). However, these three indexes were all reversed by the triptolide treatment in the test groups compared with the corresponding model groups(P<0.05). Conclusion: Triptolide may inhibit oxidase stress in diabetic nephropathy via upregulation of PRDX2 protein levels.

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 ZANG Yong,TIAN Yuan,LI Wei-dong.Triptolide affects epithelial-mesenchymal transition of renal tubular epithelial cells by regulating TGF-β1 and Hippo signaling pathways[J].Journal of Tianjin Medical University,2019,25(05):205.

备注/Memo

备注/Memo:
基金项目 天津市卫生行业2012重点攻关项目(12KG136)
作者简介 姚晶瑞(1982-),男,主治医师,硕士在读,研究方向:肾内;通信作者:姜埃利,E-mail:aili_j@163.com。
更新日期/Last Update: 2019-10-11