摘要
目的探讨丹参酮ⅡA对小鼠肺纤维化的影响及其机制。方法将A549细胞和博来霉素诱导的肺纤维化小鼠分为对照组、模型组和丹参酮ⅡA干预组,RT-PCR及Western blot检测不同组间i NOS的表达水平,ELISA检测下游TNF-α、IL-1β及IL-6的表达。结果丹参酮ⅡA干预组小鼠肺组织切片和模型组相比肺泡隔纤维增生灶减少,肺组织iNOS表达水平明显降低(P<0.05),肺灌洗液中TNF-α、IL-1β及IL-6水平明显降低(P<0.05);A549体外实验发现丹参酮ⅡA干预组较IFN-γ刺激组iNOS表达明显降低(P<0.05),细胞培养上清液中TNF-α、IL-1β及IL-6水平明显降低(P<0.05)。结论丹参酮ⅡA通过iNOS通路调控下游炎性因子的释放,从而缓解小鼠肺纤维化。
Objective To investigate the mechanism of Tanshinone ⅡA in treating with pulmonary fibrosis in mice. Methods A549 cells and Bleomycin induced pulmonary fibrosis mice were divided into control group, pulmonary fibrosis model group and Tanshinone Ⅱ A group, observe iNOS expression between different groups by PCR and western blot. Detect the down-stream cytokines TNF-α, IL-Iβ and IL-6 by using ELISA. Results Histopathology showed that puhnonary fibrosis group mice had more severe fiber foei in alveolar septum, lesions, structural damage to the lung parenchyma. The in vitro experiment showed an inhibition effect of Tanshinone Ⅱ A on iNOS expression （P 〈 0. 05）. TNF-α, IL-1β and IL-6 expression decreased significantly compared to bleomycin group （P 〈 0. 05 ）. Conclusions Tanshinone H A can reduce pulmonary fibrosis in mice by regulating iNOS expression.
出处
《基础医学与临床》
CSCD
2016年第8期1113-1117,共5页
Basic and Clinical Medicine
