Abstract: Objective To study the protective role of N-acetylsteine in the A549 cell injury caused by cigarette smoke exact and the expression change of insulin-like growth factor binding protein -3 in this process. Methods MTT assay was used to evaluate cell viability. Cell cycle and apoptotic cell proportion in each group detected respectively by PI and AnnexinV-FITC/PI double-labelled flow cytometry. Intracellular reactive oxygen species (ROS) was estimated by fluorescent indicator H2DCFDA. DAPI was used to observe the nuclear morphology. Furthermore, using real-time quantitative RT-PCR as well as western blot methods,the expression level of IGFBP-3 was detected.Result Compared with control group(0.78±0.03), CSE inhibit cell proliferation significantly(0.55±0.04). NAC can reduce cell injury caused by CSE including restoring the viability of A549 cells(0.67±0.04), attenuating G1 block of cell cycle and significantly reducing the proportion of apoptotic cells and so on. High expression of insulin-like growth factor binding protein-3 (IGFBP-3) in A549 cells treated with CSE was found at both transcriptional and protein levels, and concomitant with the restoration of cell growth after treatment with NAC, down regulation of IGFBP-3 was observed.Conclusion From the present study, it is concluded that NAC can antagonize CSE-induced growth arrest of alveolar epithelial cells and that down regulation of IGFBP-3 probably play an important role in this process.

Key words: IGFBP-3, cigarette smoke extract, alveolar epithelial cells, NAC