AIM: To study the mechanism of NAC to improve LPS induced acutelung lung injury. METHODS: The 40 rats were divided into 4 groups included NC group, Model group, NAC group and DXM group. The rats of Model, NAC and DXM groups were injected LPS, NAC group and DXM group were resepectively injected NAC (200 mg/kg) or DXM (70 mg/kg). Collecting the bronchoalveolar lavage fluid (BALF) from lung, and measuring the TGF-beta 1 concentration of BALF and lung tissue in 4 groups; After executing the rats, taken the lung tissue to observant lung pathological morphology and evaluated TGF-beta 1 expression of difference groups. Measuring the TLR-4 and NF-kappa b in 4 groups by WB assay. RESULTS: Compared with Model group, The NAC and DXM groups were improved in H& E staining, the TGF-beta 1 concentration of NAC and DXM groups were signifi cantly reduced in BALF and lung tissue (p < 0.05, respectively). TLR-4 and NF-kappa b proteins of NAC and DXM groups were lower than that of Model group in IHC and WB assays (p < 0.05, respectively). CONCLUSION: NAC had effects to protect LPS induced lung injury via TLR-4/NF-kappa b signaling pathway (Fig. 5, Ref. 19). Text in PDF www. elis. sk.