黄芩苷在流感病毒致肺纤维化早期进展中的作用机制

Mechanism of Baicalin on the early development of pulmonary fibrosis induced with FM1

目的探索黄芩苷在流感病毒感染致肺纤维化早期进展中的分子机制。方法制备甲型流感病毒性肺炎小鼠模型,用不同剂量黄芩苷溶液灌胃治疗后,观察肺指数、肺组织切片Masson染色观察纤维化程度;采用RT-PCR测定肺组织p38MARK mRNA表达,采用Western-blot测定肺组织磷酸化p38MAPK,磷酸化NF-κB-p65及TGF-β1蛋白表达。结果黄芩苷187.5、375 mg·kg-1剂量均能明显抑制肺指数及肺组织纤维蛋白的分泌;明显降低肺组织p38MAPK mRNA和蛋白表达(P<0.01);明显抑制磷酸化NF-κB-p65及TGF-β1蛋白表达(P<0.05)。结论黄芩苷抗流感病毒感染作用可能与其在肺炎致肺纤维化早期抑制纤维蛋白形成相关。

Aim To investigate the molecular mecha- nism of Baicalin （BAI） on the early development of pulmonary fibrosis induced with FM1. Methods The model of mouse influenza virus pneumonia was pre- pared. Masson staining was used to calculate lung in-dex and observe pulmonary fibrosis degree; RT-PCR was adopted to determine the mRNA expressions of p38MARK; Western blot was used to determine the protein expressions of p-p38MAPK, p-NF-KB-p65, TGF-β1. Results Compared with the model, BAI, at doses of 187.5 mg · kg-1 and 375 mg ~ kg-1, obvi- ously reduced lung index and fibrous protein secretion. It also significantly cut down mRNA expression of p38MAPK and protein expressions of p-p38MAPK, p- NF-KB-p65 and TGF-131 （ P 〈 0. 05 ）. Conclusion The effect of BAI on influenza virus infection may berelated to its suppression of fibrin formation in pneumo- nia fibrosis early stage.