[关键词]
[摘要]
目的研究复方鳖甲软肝方防治肺纤维化大鼠自由基损伤的作用和机制。方法SD雄性大鼠随机分为正常组、假手术组、模型组、强的松(0.56 m g/kg)组、复方鳖甲软肝方高、中、低剂量(1.4、0.7、0.35 g/kg)组,每组10只。除正常组、假手术组外,其余各组大鼠气管滴注盐酸博莱霉素制备大鼠肺纤维化模型。造模后第2天,各组分别ig给药,连续给药4周。测定各组大鼠肺组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(G SH-Px)、诱导型一氧化氮合酶(iNO S)活性和丙二醛(M DA)水平;采用W estern b lotting实验研究肺组织蛋白中核因子κB(NF-κB)和核因子κB抑制剂(IκBα)的表达。结果复方鳖甲软肝方能提高肺纤维化大鼠体内的G SP-Px和SOD活性,降低M DA水平和iNO S活性,减弱肺纤维化大鼠肺组织核蛋白中NF-κB表达,增强胞浆蛋白中IκBα的表达。结论复方鳖甲软肝方能调节肺纤维化大鼠体内自由基水平,减轻自由基对肺组织结构的氧化损伤,调节肺组织蛋白IκBα的表达,进而抑制NF-κB表达,是该方防治肺纤维化的作用机制。
[Key word]
[Abstract]
Objective To study effect and mechanism of Compound Biejia Ruangan Prescription (CBRP)on preventing injury of free radieal in pulmonary fibrosis rats.Methods SD male rats were randomly divided into seven groups(ten rats in each group)as normal group,Sham group,model group,prednisone group,and CBRP(1.4,0.7,0.35g/kg)groups.Rats were injected with bleomyein A5 by trachea to establish pulmonary fibrosis rat model and rats were given drugs by ig in all groups.Activities of SOD,GSH-Px,and iNOS.and MDA level in pulmonary tissues of different groups were measured.Expression of NF-κB and IκBα in protein of pulmonary tissues was studied by means of Western blotting also. Results CBRP can raise activities of GSH-Px and SOD and lessen MDA 1evel and iNOS activity.It can also downregulate the expression of NF-κB and upregulate the expression of IκBα。Conclusion CBRP can regulate the level of free radical in pulmonary fibrosis rats and lessen the oxidative injury of pulmonary tissues caused by free radical in pulmonary fibrosis rats.The mechanisms of CBRP on pulmonary fibrosis 1ie in adjusting the activity of NF-κB and further moderate that of IκBα。
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[基金项目]
国家自然科学基金项目(3054042003230130220);教育部首批非典科技攻关项目(15);教育部长江学者和创新团队发展计划资助项目(IRT0413)