[Oxidative stress induced the expression of Bax and p53 during the apoptosis of alveolar type II epithelial cell]

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2008 Feb;20(2):76-9.
[Article in Chinese]

Abstract

Objective: To investigate the effects of oxidative stress on the survival and apoptosis of alveolar epithelial type II (ATII) cells, as well as the mechanisms of apoptosis.

Methods: 500 mumol/L H(2)O(2) was added into primary ATII cells at different times and cell viability, apoptotic ratio and the expression of Bax and p53 were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry (FCM) and Western blotting analysis, respectively. The change in mitochondrial membrane potential (MMP) was detected by fluorescence microscopy and FCM.

Results: The cell viability and MMP were decreased by H(2)O(2) compared with the controls (F(1)=85.211, F(2)=72.453, respectively, both P<0.05). The cell apoptotic ratios were increased with the time of the stimulation prolonged compared with the controls (F=54.002, P<0.05). H(2)O(2) increased Bax and p53 protein levels (F(1)=28.118, F(2)=43.456, both P<0.05).

Conclusion: High level of oxidative stress can inhibit ATII cells proliferation, and induce cells apoptosis and decrease the MMP. Up-regulation of the expression of Bax and p53 may contribute to its apoptosis effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alveolar Epithelial Cells / metabolism
  • Alveolar Epithelial Cells / pathology*
  • Animals
  • Apoptosis*
  • Cell Survival
  • Cells, Cultured
  • Male
  • Membrane Potential, Mitochondrial
  • Oxidative Stress*
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Suppressor Protein p53 / metabolism*
  • bcl-2-Associated X Protein / metabolism*

Substances

  • Bax protein, rat
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein