The effect of Wogonoside on the expression of pulmonary fibrosis factor in Mycoplasma pneumoniae pneumonia
BACKGROUND Mycoplasma pneumoniae pneumonia (MPP) is an acute respiratory infectious pneumonia with pulmonary interstitial fibrosis. TGF-β1 is well accepted as the central mediator for fibrosis which promotes the formation of tissue fibrosis factor. Qinbaiqingfei pellet (Qinbai) has already been approved as the first effective new traditional Chinese medicine which can delay activities of Mycoplasma pneumoniae (M.pneumoniae) and protect lung epithelial cells in clinical trials. However, the
... . However, the mechanism of Qinbai inhibiting the expression of TGF-β1 is still unclear. METHODS The Chinese herbs in Qinbai were screened by surface plasmon resonance (SPR) and it was deteimined that Scutellaria baicalensis extracts in Qinbai showed the best binding with TGF-β1. Then the active ingredient whicn can be bound with TGF-β1 protein in the solution of Qinbai and Scutellaria baicalensis was isolated and analyzed by UPLC-Q-TOF-MS, which proved the active ingredient was Wogonoside. The affinity constant of Wogonoside and TGF-β1 protein was measured by SPR affinity analysis. A549 cells infected with M.pneumoniae were intervened by Wogonoside, and then the expression of TGF-β1 and Smad3 in A549 cells were analyzed by PCR and western blotting. RESULTS The results showed the bound effect of Scutellaria baicalensis and TGF-β1 was effective. The active ingredients which can be bound with TGF-β1 in the solution of Scutellaria baicalensis and Qinbai were obtained and analyzed to investigate the mechanism of Qinbai inhibiting the expression of TGF-β1. UPLC-Q-TOF-MS results showed that the active ingredients was Wogonoside. SPR affinity analysis showed that the affinity constant was 21.71 µM. Pharmacological experiments revealed that Wogonoside strongly inhibited the expression of TGF-β1 and Smad3 in A549 cells infected by M.pneumoniae. CONCLUSION Wogonoside in Qinbai can be bound with TGF-β1 and down-regulate the expression of lung fibrosis factors TGF-β1 and Smad3. The finding may improve our understanding the molecular mechanism of Qinbai mediating MPP and provide new sights into the future pharmacological investigation of Qinbai.