Tiaobufeishen decoction could decrease the expression of the caveolin-1, p-p38, MMP3, inhibit the activation of the caveolin-1-p38MAPK signaling pathway.
Objective: Reliving the relationship of the Caveolin-1-p38 MAPK signaling pathway and COPD tracheobronchomalacia, and research the mechanism of Tiaobufeishen decoction improve the regression of the weasand cartilage cells.Methods Flow cytometry was used to analyze the apoptosis rate to determine the optimal concentration of Tiaobufeishen decoction and CSE, CCK8 assay was used to determine the optimal concentration of P38-MAPK specific inhibitor. The COPD cell model was created by tracheal chondrocyte which dispose by optimal concentration CSE, then add the IL-1β set up the chondrocyte degeneration model, use the method of toluidine blue staining and immunohistochemical authenticate degeneration of cartilage. This research included control group, model group, model-Tiaobufeishen group, model-blocker group. When the model was set up succeed, add the Tiaobufeishen decoction and P38-MAPK blocker in the model-Tiaobufeishen and model-blocker groups, respectively. Western Blot was used to detect the expression of caveolin-1 and p-p38 in the chondrocyte. RT-PCR was used to detect the expression of MMP3 and caveolin-1 in the matrix.Results The cell activity was not influence by the concentration of Tiaobufeishen decoction and blocker, the concentration of the CSE model was moderation. Compared with control group, the level of caveolin-1, p38MAPK, MMP3 in the model group was significant increase, moreover, the result of toluidine blue staining and immunohistochemical methods show that the chondrocyte has obvious regression. The expression of caveolin-1, p38MAPK, and MMP3 have significant decrease than the control group, and the reduction of chondrocyte degeneration.Conclusion The caveolin-1-p38MAPK signaling pathway play an important role in the morbidity of the tracheobronchomalacia. Tiaobufeishen decoction could decrease the expression of the caveolin-1, p-p38, MMP3, inhibit the activation of the caveolin-1-p38MAPK signaling pathway, therefore, it can improve the tracheobronchomalacia.