Objective  To explore the effect of oxidative stress on the activation of mitogen activated protein kinases (MAPKs) in alveolar type II  epithelial cells (AT II) and the protective role of N-acetylcysteine (NAC) in this induced damage.   Methods  Primary rat AT II cells were randomly divided into 4 groups

control

NAC (5 mmol/L)

H

2

O

2

(500 μmol/L)

H

2

O

2

plus NAC pretreatment groups. The morphological change of AT II cells was observed under transmitting electron microscopy (TEM) after H

2

O

2

stimulation. Cell viability was assessed with 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT). Apoptotic ratio and intracellular reactive oxygen species (ROS) levels were measured by flow cytometry. The phosphorylation of ERK

p38 and JNK were analyzed by Western blotting.   Results  The typical apoptosis was observed in the cells after H

2

O

2

  stimulation. Decreased cell viability

increased intracellular ROS and apoptotic ratio were observed after the stimulation of H

2

O

2

  (P0.05). Pretreatment with NAC improved cell viability

decreased intracellular ROS levels and apoptosis (P0.05). NAC attenuated the phosphorylation of ERK

p38 and JNK induced by H

2

O

2

  (P0.05).   Conclusion  H

2

O

2

activates MAPKs and induces apoptosis in ATⅡ cells. NAC attenuates cells apoptosis through eliminating intracellular ROS and inhibiting the activation of MAPKs.