CAJ | 학술논문

目的：研究acsdKP对硅肺纤维化大鼠肺内nf-κB p65表达的影响。方法大鼠随机分三组：对照组：支气管内灌注生理盐水1ml/只。硅肺模型组：支气管内灌注sio2混悬液1ml/只。acsdKP治疗组：支气管内灌注sio2混悬液1ml/只，并持续给大鼠acsdK药物治疗。各组大鼠都在8周后处死。用Western blot法检测大鼠肺组织中nf-κB p65的表达情况。结果在硅肺模型组中，nf-κB p65蛋白的表达较对照组上升。经过acsdKP治疗后，nf-κB p65蛋白的表达较硅肺模型组下降。结论acsdKP可能使iκB的稳定性增加，进而nf-κB p65失活，抑制肺泡炎和纤维化的发生发展。
목적：연구acsdKP대규폐섬유화대서폐내nf-κB p65표체적영향。방법대서수궤분삼조：대조조：지기관내관주생리염수1ml/지。규폐모형조：지기관내관주sio2혼현액1ml/지。acsdKP치료조：지기관내관주sio2혼현액1ml/지，병지속급대서acsdK약물치료。각조대서도재8주후처사。용Western blot법검측대서폐조직중nf-κB p65적표체정황。결과재규폐모형조중，nf-κB p65단백적표체교대조조상승。경과acsdKP치료후，nf-κB p65단백적표체교규폐모형조하강。결론acsdKP가능사iκB적은정성증가，진이nf-κB p65실활，억제폐포염화섬유화적발생발전。
ObjectiveTo investigate the effect of AcSDKP on the expression of NF-κB p65 pulmonary fibrosis in rats. Methods the rats were randomly divided into 3 groups, control group with bronchial infusion of saline solution with 1ml, model group with bronchial infusion of sio2 injectable suspension with 1 ml and treatment group treated with consecutive AcSDKP on the basis of model made in the model group. After rats in each group were killed, the expression of NF-κB p65 was detected by Western blot.Results The expression of NF-κB p65 increased in the silicosis model group. After treated by AcSDKP, the expression of NF-κB p65 decreased in the treatment group.Conclusion AcSDKP could inactivate NF-κB p65 by strengthening stability of IκB, which may inhibit alveolar inlfammation and the occurrence and development of ifbrosis.