PROTECTIVE EFFECT OF N-ACETYLCYSTEINE ON HYPEROXIA-INDUCED LUNG INJURY AND ITS INTERACTION WITH P38 MITOGEN-ACTIVATED PROTEIN KINASE SIGNALING PATHWAY

INTRODUCTION: N -Acetylcysteine (NAC) is an effective oxidation inhibitor, but the protection of NAC in hyperoxia-induced lung injury is unknown. OBJECTIVE: The objective of this study was to explore the protective effect of NAC on hyperoxia-induced lung injury and change of p38 mitogen-activated protein kinase (MAPK) expression caused by NAC treatment. METHODS: Forty Wistar rats were randomly assigned to room air (A), hyperoxia injury (B), hyperoxia + NAC (C), hyperoxia + SB203580 (D), or hyperoxia + NAC + SB203580 (E). The lung wet/dry ratio, pathology, and location and quantity of p38 protein were detected. RESULTS: Although pathologic changes in group B included severe alveolar edema with inflammatory cell aggregation and red blood cell leakage, the lung micrographic pictures in groups C, D, and E were improved significantly compared with group B; p38-positive cells increased in group B compared with that in group A and labeled in many types cells in lung tissue, especially in infiltrative inflammatory cells. In groups C, D, and E, the positive cells remarkably decreased compared with those in group B; the quantity of p38 MAPK was higher in group B than in group A, and p38 expression in groups C, D, and E decreased significantly compared with group B but was higher than that in the control group. There was no significant difference of p38 quantity among the 3 groups. CONCLUSIONS: Reactive oxygen species activated phospho-p38 MAPK signaling pathway, and NAC and SB203580 treatments reduced the extent of hyperoxia-induced lung injury, as evidenced by reduction of the wet/dry ratio and lung pathology. NAC may exert a protective effect on hyperoxia-induced lung injury through attenuation of reactive oxygen species–induced p38 MAPK activation.