N-acetylcysteine protects alveolar epithelial cells from hydrogen peroxide-induced apoptosis through scavenging reactive oxygen species and suppressing c-Jun N-terminal kinase

作者：Fu, Yue-qiang; Fang, Fang; Lu, Zhong-yi; Kuang, Feng-wu; Xu, Feng^*

来源：Experimental Lung Research, 2010, 36(6): 352-361.

DOI：10.3109/01902141003678582

• alveolar type II epithelial cells
• apoptosis
• cytoprotective properties
• JNK
• NAC
• reactive oxygen species

The production of reactive oxygen species (ROS) during hyperoxia contribute to alveolar epithelial apoptosis. In the present study, the molecular mechanisms of oxidative stress-induced alveolar epithelial cell apoptosis were investigated. The cytoprotective effects of N-acetylcysteine (NAC) were evaluated. Treatments using 500 mu M H2O2 can induce primary alveolar type II epithelial cell apoptosis. During this procedure, c-Jun N-terminal kinase (JNK) was activated. SP600125, a specific inhibitor of JNK, can partially block H2O2-induced alveolar type II epithelial cells (ATII cells). SP600125 also attenuated Bax protein content and p53 nuclear accumulation induced by H2O2. NAC (5 mM) pretreatment decreased H2O2-induced ATII cell apoptosis. The high level of intracellular reactive oxygen species (ROS) induced by H2O2 was also attenuated by NAC pretreatment. Taken together, H2O2 can induce primary ATII cells apoptosis and increase JNK phosphorylation. NAC, a precursor of glutathione (GSH) synthesis, can protect ATII cells from H2O2-induced apoptosis through scavenging ROS.

• 出版日期2010-8
• 单位重庆医科大学; 南京医科大学