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硫化氢激活H9c2心肌细胞容积调节性氯通道

杨春涛 左婉红 赵斌 赵磊 蔡典其 陈丽新 王立伟 冯鉴强 廖新学

中国动脉硬化杂志2012,Vol.20Issue(6):523-527,5.
中国动脉硬化杂志2012,Vol.20Issue(6):523-527,5.

硫化氢激活H9c2心肌细胞容积调节性氯通道

Hydrogen Sulfide Activated Volume-Regulated Chloride Channel in H9c2 Cardiomyocytes

杨春涛 1左婉红 2赵斌 3赵磊 1蔡典其 1陈丽新 2王立伟 2冯鉴强 4廖新学3

作者信息

  • 1. 广州医学院生理学教研室,广东省广州市510182
  • 2. 暨南大学医学院生理学教研室,广东省广州市510632
  • 3. 中山大学附属第一医院心血管内科,广东省广州市510080
  • 4. 中山大学中山医学院生理学教研室,广东省广州市510080
  • 折叠

摘要

Abstract

Aim To investigate the effect of hydrogen sulfide (H2S) on volume-regulated chloride channel (VRCC). Methods H9c2 cardiomyoeytes were cultured and treated with sodium hydrosulfide (NaHS, a H2S donor). Expression of C1C-3 protein and VRCC chloride current (/c-VRCc) were measured by Western blot assay and whole cell patch clamp, respectively. Results When H9c2 cardiomyocytes were placed in the isotonic solution, la was slightly activated. Hypotonicity obviously enhanced la(P<0. 01) , which was statistically attenuated by hypertonicity (P <0. 05). C1C-3 protein was expressed in H9c2 cardiomyocytes. Similarly to the effect of isohylonicity on the activation of VRCC, treatment with 400 jimol/L NaHS for 0-30 min significantly increased /CIVRCC(P<:0. 01), which was also statistically attenuated by hypertonicity (P < 0.05). However, treatment with 400 ujnol/L NaHS for 0 - 30 min did not alter the expression of C1C-3 protein in H9c2 cardiomyocytes (P > 0. 05). Conclusions Both VRCC and C1C-3 protein were expressed in H9c2 cardiomyocytes. H2S activated VRCC in a ClC-3-independent manner.

关键词

硫化氢/容积调节性氯通道/ClC-3氯通道蛋白/H9c2心肌细胞

Key words

Hydrogen Sulfide/Volume-Regulated Chloride Channel/C1C-3 Protein/H9e2 Cardiomyocytes

分类

生物科学

引用本文复制引用

杨春涛,左婉红,赵斌,赵磊,蔡典其,陈丽新,王立伟,冯鉴强,廖新学..硫化氢激活H9c2心肌细胞容积调节性氯通道[J].中国动脉硬化杂志,2012,20(6):523-527,5.

基金项目

广东省科技计划项目(2009B080701014) (2009B080701014)

中国动脉硬化杂志

OA北大核心CSCDCSTPCD

1007-3949

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