A role of sodium selenite in regulating expression of p38 mitogen-activated protein kinase (p38MAPK) and vascular endothelial growth factor (VEGF)in rat mesangial cells

WEI Qianping; et al

doi:10.13406/j.cnki.cyxb.2005.02.008

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A role of sodium selenite in regulating expression of p38 mitogen-activated protein kinase (p38MAPK) and vascular endothelial growth factor (VEGF)in rat mesangial cells

更新时间：2024-01-17

- A role of sodium selenite in regulating expression of p38 mitogen-activated protein kinase (p38MAPK) and vascular endothelial growth factor (VEGF)in rat mesangial cells
- Journal of Chongqing Medical University Issue 2, Pages: 191-195(2005)
- 作者机构：
  
  1. 重庆医科大学临床学院内分泌科
  2. 重庆医科大学超声工程研究所,重庆,400016
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2005.02.008
  CLC： R587.24
- Published：2005，
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[1]魏倩萍,邓华聪,赵劼.亚硒酸钠对大鼠肾小球系膜细胞p38MAPK和VEGF表达的调控[J].重庆医科大学学报,2005(02):191-195+199.

WEI Qianping, et al. A role of sodium selenite in regulating expression of p38 mitogen-activated protein kinase (p38MAPK) and vascular endothelial growth factor (VEGF)in rat mesangial cells. [J]. Journal of Chongqing Medical University (2):191-195(2005)
[1]魏倩萍,邓华聪,赵劼.亚硒酸钠对大鼠肾小球系膜细胞p38MAPK和VEGF表达的调控[J].重庆医科大学学报,2005(02):191-195+199. DOI： 10.13406/j.cnki.cyxb.2005.02.008.

WEI Qianping, et al. A role of sodium selenite in regulating expression of p38 mitogen-activated protein kinase (p38MAPK) and vascular endothelial growth factor (VEGF)in rat mesangial cells. [J]. Journal of Chongqing Medical University (2):191-195(2005) DOI： 10.13406/j.cnki.cyxb.2005.02.008.

摘要

目的:探讨丝裂素活化蛋白激酶p38（ p38MAPK ）和血管内皮生长因子（VEGF）的关系

从而研究p38MAPK和VEGF在糖尿病肾病中的作用及硒在抗糖尿病肾病中的作用机制。方法:分别以高葡萄糖、糖基化终产物

高胰岛素和过氧化氢孵育大鼠肾小球系膜细胞（RMCs） ;以p38MAPK特异抑制剂SB2 0 35 80和亚硒酸钠分别预处理RMCs

再给予上述四种刺激因素孵育RMCs

观察RMCsp38MAPK和VEGF蛋白表达。结果:高葡萄糖、糖基化终产物、高胰岛素和过氧化氢均可独立激活p38MAPK

使其磷酸化表达量增加

VEGF表达也明显增加:SB2 0 35 80预处理后

VEGF表达被显著抑制;亚硒酸钠预处理后

p38MAPK磷酸化被明显抑制

同时VEGF表达显著降低。结论:p38MAPK调控VEGF的表达

表明p38MAPK和VEGF参与了糖尿病肾病的发生发展;亚硒酸钠可通过抑制p38信号通路而抑制VEGF的表达

从而有效地防治糖尿病肾病。

Abstract

Objective:To investigate the relationship between p38 mitogen-activated protein kinase(p38MAPK) and vascular endothelial growth factor (VEGF)

and to study the role of p38 mitogen-activated protein kinase and vascular endothelial growth factor for diabetic nephropathy

and therefore to study the mechanism of sodium selenite in anti-diabetic nephropathy.Methods:We initially investigated protein expression of p38MAPK and VEGF in rat mesangial cells(RMCs)which were incubated respectively with 25 mmol/L glucose

100mg/L BSA-AGEs

100nmol/L insulin and 100 μmol/L H 2O 2.We also studied the relationship between p38MAPK and VEGF protein expression by using SB203580

a specific inhibitor of p38MAPK.We then evaluated the direct effects of sodium selenite on the regulation of p38MAPK and VEGF protein expression.Results:p38MAPK and VEGF had significantly higher expression in RMCs incubated with 25mmol/L glucose

100mg/L BSA-AGEs

100nmol/L insulin and 100μmol/L H 2O 2 respectively.VEGF activity was significantly reduced when p38MAPK was inhibited by SB203580.Furthermore

both p38MAPK and VEGF protein expression were significantly decreased in RMCs with sodium selenite treatment.Conclusion:p38MAPK and VEGF are involved in development of diabetic nephropathy and p38MAPK stimulation is essential for VEGF expression

and also suggests that sodium selenite may play a role in the prevention of diabetic nephropathy by down-regulation of both p38MAPK and VEGF expression.

关键词

亚硒酸钠p38MAPKVEGF糖尿病肾病大鼠肾小球系膜细胞

Keywords

Sodium seleniteP38 mitogen-activated protein kinasevascular endothelial growth factordiabetic nephropathyRat mesangial cells

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