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首页|期刊导航|南京医科大学学报(自然科学版)|LXA4通过p38MAPK/Nrf2信号通路诱导H9c2心肌细胞HO-1高表达

LXA4通过p38MAPK/Nrf2信号通路诱导H9c2心肌细胞HO-1高表达

周昱 吴升华 陈筱青 唐艳荣

南京医科大学学报(自然科学版)2012,Vol.32Issue(11):1493-1498,6.
南京医科大学学报(自然科学版)2012,Vol.32Issue(11):1493-1498,6.

LXA4通过p38MAPK/Nrf2信号通路诱导H9c2心肌细胞HO-1高表达

LXA4 increases the expression of HO-1 by activation of p38MAPK/Nrf2 pathway in H9c2 cardiomyocytes

周昱 1吴升华 1陈筱青 1唐艳荣1

作者信息

  • 1. 南京医科大学第一附属医院儿科,江苏南京210029
  • 折叠

摘要

Abstract

Objective:To investigate the possible mechanisms of signal transduction pathways of heme oxygenase (HO)-1 expression induced by lipoxin A4 (LXA4) in H9c2 cardiomyocytes. Methods:H9c2 cells were exposed to hypoxia followed by reoxygenation with or without pretreatment of LXA4,nuclear factor-E2 related factor 2(Nrf2) inhibitor (ATRA),p38MAPK inhibitor (SB203580),LXA4 combined with ATRA,and LXA4 combined with SB203580. The mRNA transcription and protein expression of HO-1,Nrf2 and p38MAPK was examined by RT-PCR, Western blot and immunofluorescence staining. Results: Compared with hypoxia/reoxygenation group,the mRNA transcription and protein expression of H0-1 in H9c2 cardiomyocytes pretreated with LXA4 increased significantly(P < 0.05). The expression of HO-1 in H9c2 cardiomyocytes decreased (P < 0.05) after treated with ATRA or SB203580. ATRA blocked the nuclear accumulation of Nrf2 and decreased HO-1 protein expression induced by LXA4 pretreatment (P < 0.05). SB203580 inhibited the phosphorylation level of p38MAPK and decreased HO-1 protein expression induced by LXA4 pretreatment(P < 0.05). Conclusion: LXA4 can induce HO-1 over-expression which has protective effect on H9c2 cardiomyocytes of hypoxia/reoxygenation injury. Its mechanism is related to p38MAPK/Nrf2 signal transduction pathways.

关键词

脂氧素/血红素加氧酶/核因子E2相关因子2/p38MAPK/缺氧/复氧损伤

Key words

lipoxins/heme oxygenase/nuclear factor-E2 related factor 2/p38MAPK/hypoxia/reoxygenation injury

分类

生物科学

引用本文复制引用

周昱,吴升华,陈筱青,唐艳荣..LXA4通过p38MAPK/Nrf2信号通路诱导H9c2心肌细胞HO-1高表达[J].南京医科大学学报(自然科学版),2012,32(11):1493-1498,6.

基金项目

国家自然科学基金(30973534,81173052) (30973534,81173052)

南京医科大学学报(自然科学版)

OA北大核心CSCDCSTPCD

1007-4368

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