Effects of uncoupling protein 2 on cardiomyocyte hypertrophy induced by indoxyl sulfate

徐新丽; 杨可; 管旭; 肖堂利; 何婷; 余彦琳; 刘亮; 赵景宏

您当前的位置：

首页 >

文章列表页 >

Effects of uncoupling protein 2 on cardiomyocyte hypertrophy induced by indoxyl sulfate

更新时间：2026-01-09

- Effects of uncoupling protein 2 on cardiomyocyte hypertrophy induced by indoxyl sulfate
- Journal of Army Medical University Vol. 36, Issue 22, Pages: 2277-2282(2014)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  CLC： R341;R363.21;R542.2
- Published：2014
- 稿件说明：
移动端阅览
徐新丽,杨可,管旭,肖堂利,何婷,余彦琳,刘亮,赵景宏.UCP2在硫酸吲哚酚诱导心肌细胞肥大中的作用[J].陆军军医大学学报(原第三军医大学学报),2014,36(22):2277-2282.

　Xu Xinli,Yang Ke,Guan Xu,Xiao Tangli,He Ting,Yu Yanlin,Liu Liang,Zhao Jinghong.Effects of uncoupling protein 2 on cardiomyocyte hypertrophy induced by indoxyl sulfate[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(22):2277-2282.
徐新丽,杨可,管旭,肖堂利,何婷,余彦琳,刘亮,赵景宏.UCP2在硫酸吲哚酚诱导心肌细胞肥大中的作用[J].陆军军医大学学报(原第三军医大学学报),2014,36(22):2277-2282. DOI：

　Xu Xinli,Yang Ke,Guan Xu,Xiao Tangli,He Ting,Yu Yanlin,Liu Liang,Zhao Jinghong.Effects of uncoupling protein 2 on cardiomyocyte hypertrophy induced by indoxyl sulfate[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(22):2277-2282. DOI：

摘要

目的探讨解耦联蛋白2（uncoupling protein 2

UCP2）在硫酸吲哚酚（indoxyl sulfate，IS）诱导心肌细胞肥大中的作用和机制。方法分离培养新生Sprague-Dawley大鼠心肌细胞，0、100、250、500、1 000 μmol/L IS孵育心肌细胞1 h或500 μmol/L IS孵育心肌细胞0、15、30、45、60 min后，Western blot检测心肌细胞UCP2蛋白表达变化。UCP2慢病毒转染心肌细胞后，通过α-actinin免疫荧光染色观察细胞大小，

H-亮氨酸掺入法评价蛋白合成速率，Real-time PCR检测肥大相关基因ANF、BNP和β-MHC mRNA的表达，同时利用Mitosox

探针检测活性氧(reactive oxygen species

ROS)生成情况。结果与对照组相比，IS处理组心肌细胞的UCP2蛋白水平明显下降（P0.05）；与IS处理组相比，UCP2过表达可以明显抑制IS诱导的心肌细胞ROS生成、体积增大、

H-亮氨酸摄入增加及肥大相关基因（ANF、BNP和β-MHC mRNA）的表达增高，差异有统计学意义（P0.05）。结论 IS诱导心肌细胞肥大可能与其下调UCP2表达及促进氧化应激有关，而UCP2过表达或许可以通过抑制氧化应激拮抗IS诱导的心肌细胞肥大。

Abstract

Objective To investigate the effects of uncoupling protein 2 (UCP2) on cardiomyocyte hypertrophy induced by indoxyl sulfate (IS). Methods Neonatal rat cardiomyocytes were separately treated with IS of 0

100

250

500

and 1 000 μmol/L for 1 h or with 500 μmol/L IS for 0

and 60 min. Then UCP2 expression was tested with Western blotting. After neonatal rat cardiomyocytes were infected with lentivirus

we observed the expressio

n of UCP2 by Western blotting and detected reactive oxygen species (ROS) production by Mitosox

. Cell size was tested by immunofluorescent staining of α-actinin. ANF

BNP and β-MHC mRNA and [

]

leucine incorporation were examined as indicators of cardiomyocyte hypertrophy. Results Compared with the control group

IS treatment reduced the expression of UCP2 in a dose- and time-dependent manner (P0.05). UCP2 overexpression significantly suppressed ROS generation

inhibited the increase of cell volume and [

]

leucine incorporation

and reduced the mRNA expression of ANF

BNP

and β-MHC induced by IS (P0.05). Conclusion IS may induce cardiomyocyte hypertrophy by down-regulating UCP2 expression and enhancing oxidative stress. UCP2 overexpression may antagonize IS-induced cardiomyocyte hypertrophy by inhibiting oxidative stress.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

FLI-1 ameliorates cardiac hypertrophy by inhibiting IGF-1R/Gi/PLC pathway via up-regulation of Klotho

G protein-coupled bile acid receptor 1 activation attenuates endothelin-1-induced rat cardiomyocyte hypertrophy by inhibiting CaN/NAFT3 pathway

Effect of albumin-bound indoxyl sulfate on the chemotaxis in monocytes

Indoxyl sulfate induces renal fibrosis in mice

Albumin-bound indoxyl sulfate damages erythrocytes in vitro

Related Author

司良毅

龙军

钟理

王维维

唐刚

冯健

李家富

陈德秀

Related Institution

No data

⁰