No abstract

AIM: Platycodin D (PD), an oleanane kind of triterpenoid saponin, possesses various pharmacological activities. We aimed to investigate the effects of PD in pulmonary fi brosis. METHOD: MRC-5 cells were induced by transforming growth factor-beta1 (TGF-β1) to simulate the pulmonary fi brosis in vitro. Cell viability was determined using a CCK-8 kit in the absence or presence of PD. Then, the expression of proliferation-related proteins was detected using immunofl uorescence assay or western blot analysis. Moreover, the levels of infl ammatory factors were examined. Subsequently, the ability of cell migration was evaluated using wound healing assay. Additionally, western blot analysis was employed to determine migration-and extracellular matrix accumulation (ECM)-related proteins expression. RESULTS: Results indicated that PD exposure signifi cantly dose-dependently inhibited TGF-β1 induced proliferation in MRC-5 cells. Additionally, the contents of infl ammatory factors were notably inhibited with PD treatment. Furthermore, signifi cant decrease in migration of TGF-β1-stimulated MRC-5 cells was observed after PD intervention. Afterwards, PD remarkably suppressed the expression of alpha smooth muscle actin (α-SMA), collagen I (Col I), collagen III (Col III) and E-cadherin (E-cad). CONCLUSIONS: PD attenuated proliferation and ECM accumulation in TGF-β1 induced lung fi broblasts, providing experimental support for the clinical application of PD in the treatment of pulmonary fi brosis (Fig. 6, Ref. 33).