羟基红花黄色素A抑制高糖诱导的小鼠肾足细胞损伤

基础医学与临床 ›› 2021, Vol. 41 ›› Issue (1): 27-32.

羟基红花黄色素A抑制高糖诱导的小鼠肾足细胞损伤

谢飞¹, 周美兰^2*

1.武警陕西省总队医院内一科, 陕西西安 710054;
2.空军军医大学第一附属医院肾脏内科, 陕西西安 710032

收稿日期:2019-12-31 修回日期:2020-05-10 出版日期:2021-01-05 发布日期:2020-12-30
通讯作者: ^*euqwd26@163.com
基金资助:
国家自然科学基金(81470993)

Hydroxysafflor yellow A inhibits high glucose-induced renal podocyte injury of mice

XIE Fei¹, ZHOU Mei-lan^2*

1. Department of Internal Medicine,Shaanxi Armed Police Corps Hospital,Xi'an 710054;
2. Department of Kidney Internal Medicine, the First Affiliated Hospital of the Air Force Medical University,Xi'an 710032, China

Received:2019-12-31 Revised:2020-05-10 Online:2021-01-05 Published:2020-12-30
Contact: ^*euqwd26@163.com

摘要/Abstract

摘要： 目的探讨羟基红花黄色素A(HYSA)对高糖(HG)诱导的小鼠足细胞损伤的影响及其机制。方法将体外培养的小鼠肾足细胞系MCP5分为对照组、HG组、HG+HYSA-L组、HG+HYSA-M组和HG+HYSA-H组;采用CCK-8法检测细胞活力;流式细胞测量术检测细胞凋亡;比色法检测细胞caspase-3活性;相关试剂盒检测细胞内MDA、SOD和GSH-PX含量,Western blot检测细胞中nephrin、fibronectin、α-SMA、VEGF蛋白表达和JNK磷酸化水平。结果与对照组比较,HG组细胞存活率、nephrin表达水平和SOD、GSH-PX含量明显降低(P＜0.05);凋亡率、caspase-3活性、MDA含量和fibronectin、α-SMA、VEGF蛋白表达水平以及JNK磷酸化水平明显升高(P＜0.05);与HG组比较,HYSA可呈浓度依赖性逆转HG引起的上述变化(P＜0.05)。结论 HYSA可通过抑制高糖诱导的细胞凋亡、上皮间质转化和氧化应激反应保护足细胞损伤,其作用机制可能与抑制JNK信号通路活化和VEGF蛋白表达有关。

关键词: 糖尿病肾病, 足细胞, 凋亡, 氧化应激, JNK信号通路

Abstract: Objective To investigate the effect of hydroxysafflor yellow A (HYSA) on high glucose (HG)-induced podocyte injury of mice and its mechanism. Methods Cultured podocytes(MCP5) were divided into control group, HG group, HG+HYSA-L group, HG+HYSA-M group and HG+HYSA-H group. Cell viability was detected by CCK-8 method, cell apoptosis was detected by flow cytometry, caspase-3 activity was detected by colorimeter, MDA, SOD and GSH-Px content in cells were detected by kit, the expression of nephrin, fibronectin, α-SMA, VEGF protein and JNK phosphorylation level in cells was detected by Western blot. Results Compared with the control group, the cell survival rate, nephrin protein expression, SOD, GSH-Px content of HG group were significantly reduced, apoptosis rate, caspase-3 activity, MDA content, fibronectin, α-SMA, VEGF protein expression and JNK phosphorylation were all significantly increased (P＜0.05); compared with HG group, HYSA reversed the above changes caused by HG with a concentration dependent manner (P＜0.05). Conclusions HYSA protects podocytes agains high glucose-induced injury by inhibiting apoptosis, epithelial-mesenchymal transformation and oxidative stress. Its mechanism is potentially related to the inhibition of JNK signal pathway activation and VEGF protein expression.

Key words: diabetic nephropathy, podocyte, apoptosis, oxidative stress, JNK signaling pathway

中图分类号:

R692

谢飞, 周美兰. 羟基红花黄色素A抑制高糖诱导的小鼠肾足细胞损伤[J]. 基础医学与临床, 2021, 41(1): 27-32.

XIE Fei, ZHOU Mei-lan. Hydroxysafflor yellow A inhibits high glucose-induced renal podocyte injury of mice[J]. Basic & Clinical Medicine, 2021, 41(1): 27-32.

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