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Calpain抑制剂ALLN对H2O2诱导的661W细胞损害的影响

方丽君 林颖彬 黄恩 黄天文

中国药理学通报2018,Vol.34Issue(2):181-185,5.
中国药理学通报2018,Vol.34Issue(2):181-185,5.DOI:10.3969/j.issn.1001-1978.2018.02.008

Calpain抑制剂ALLN对H2O2诱导的661W细胞损害的影响

Possible effect of N-acetyl-leu-leu-norleucinal, an inhibitor of Calpain, on H2O2-induced damage in 661W cells

方丽君 1林颖彬 2黄恩 3黄天文4

作者信息

  • 1. 福建医科大学附属协和医院眼科,福建福州350001
  • 2. 福建医科大学附属协和医院福建省老年医学研究所,福建福州350001
  • 3. 福建省老年医学研究所,福建福州350001
  • 4. 加拿大渥太华大学医学院细胞分子医学系,渥太华K1H 8M5
  • 折叠

摘要

Abstract

Aim To investigate the possible effect of N-acetyl-leu-leu-norleucinal (ALLN),an inhibitor of Calpain,on H2O2-induced damage in 661W cells.Methods The cellular survival of 661W treated with different doses of H2O2 without or with ALLN for 24 h was measured by MTT assay.The protein level of Calpain 1 and Calpain 2 was assessed by Western blot.Results Upon the H2O2 treatment at the concentrations of 50,100,500,1 000 μmol · L-1,the survival rate of 661W significantly decreased in a dose-dependent manner compared to that of the control group.Furthermore,the protein level of Calpain 1 and Calpain 2 showed an obviously time-dependent increase in 661W cells treated with 100 μmol · L-1 H2O2 for 12,18,24 h.Finally,the survival rate of 661W treated with ALLN and H2O2 was higher than that treated only with H2O2,and there was no difference in survival rate between ALLN groups (at the concentrations of 25,50,100,200 μmol · L-1) and control group.Conclusions Calpain is involved in the damage induced by H2O2.ALLN,the inhibitor of Calpain,attenuates the oxidative damage,which plays a promising protective role in photo-receptor cells under oxidative stress.

关键词

ALLN/661W/H2O2/Calpain蛋白/光感受器细胞/视网膜色素变性

Key words

N-acetyl-leu-leu-norleucinal/661W/H2O2/Calpain protein/photo-receptor cells/retinitis pigmentosa

分类

医药卫生

引用本文复制引用

方丽君,林颖彬,黄恩,黄天文..Calpain抑制剂ALLN对H2O2诱导的661W细胞损害的影响[J].中国药理学通报,2018,34(2):181-185,5.

基金项目

国家自然科学基金资助项目(No 81100812) (No 81100812)

福建省自然科学基金资助项目(No 2017J01292) (No 2017J01292)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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