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AIM: Acute lung injury (ALI) is associated with excessive inflammation caused by high TNF-α concentration.We hypothesized that anti-TNF-α therapy would have beneficial effects in experimental ALI in mice via oxidative stress inhibition.METHODS: LPS (5mg/Kg) was intratracheally administered to the BALB/c mice (8-10 week old).Before LPS treatment, mice were given TNFR-Fc intraperitoneally once at a dose of 0.4mg/Kg.On 0 and 2 hour after LPS treatment, animals were sacrificed respectively.Lung histology was introduced to evaluate lung injury.TNF-α concentration in serum, MDA and total anti-oxidative stability were assayed.Finally, the transcription level of iNOS, Nox1, Nox2 and Nox4 were evaluated by qRT-PCR.RESULTS: TNFR-Fc treatment decreased serum TNF-α concentration significantly (P<0.001) as well as the score of the lung histology (P<0.001).ALI mice treated with TNFR-Fc hit a lower transcription level ofNox1, Nox2 and Nox4 XO (P=0.011, P=0.011, P=0.021).The total anti-oxidative stability of mice treated with TNFR-Fc was preserved better than those treated with LPS alone (P=0.034).CONCLUSION: Treatment with TNFR-Fc significantly reduced LPS-induced ALI.The transcription level of Nox was down-regulate by anti-TNF-α therapy, following by oxidative stress attenuation.