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Objective:To evaluate the protective effects of Reduning Injection(热毒宁注射液.RON),a patent Chinese medicine,on lipopolysaccharide(LPS)-induced acute lung injury(ALI)in rats and its underlying mechanisms of action.Methods:Sixty male Sprague-Dawley rats were randomly divided into 6 groups,including normal control,model,dexamethasone(DEX,5 mg/kg),RDN-H(720 mg/kg),RDN-M(360 mg/kg)and RDN-L(180 mg/kg)groups,with 10 rats in each group.Rats were challenged with intravenous injection of LPS 1 h after intraperitoneal treatment with RDN or DEX.At 6 h after LPS challenge,lung tissues and bronchoaiveolar lavage fluid(BALF)were collected,and the number of inflammatory cells was determined.The right lungs were collected for histopathologic examination,measurement of gene and protein expressions,superoxide dismutase(SOD)and myeloperoxidase(MPO)activities.Results:In vivo pretreatment of RDN(360,720 mg/kg)significantly reduced the weight of wet to dry(W/D)ratio of lung,protein content in BALF,and led to remarkable attenuation of LPS-induced histopathological changes in the lungs.Meanwhile,RDN enormously decreased BALF total inflammatory cells,especially neutrophil and macrophage cell numbers.Moreover,RDN increased SOD activity,inhibited MPO activity,alleviated LPS-induced tumor neurosis factor-α(TNF-α)and inducible nitric oxide synthase(iNOS)expression in lung tissues.Furthermore,RDN(720 mg/kg)efficiently weakened nuclear factorkappa B(NF-κB)gene and protein expression.Conclusion:Anti-inflammatory effects of RDN was demonstrated to be preventing pulmonary neutrophil infiltration,lowering MPO activity,TNF-αand iNOS gene expression by inhibiting NF-κB activity in LPS-induced ALI.