Cortex Dictamni extracts inhibit over-proliferation and migration of rat airway smooth muscle cells via FAK/p38/Bcl-2 signaling pathway.

Airway smooth muscle (ASM) is a prominent effecter in maintaining bronchial muscle contraction and responsible for airway hyper-responsiveness (AHR); the phenotype change and over-proliferation of airway smooth muscle cells (ASMCs) play key roles in the pathogenesis of asthma. The aim of this study was to investigate the anti-proliferation effects of Cortex Dictamni aqueous extract (CDAE) and ethanol extract (CDE) on ASMCs and the possible underline mechanisms. Cell proliferation rates were determined by MTT assay; matrix metalloproteinases-2 (MMP-2) activity was examined by gelatin zymography; cell proliferation and migration were appraised by in-vitro cell-gap closure assessment; protein expressions of p38, Bcl-2 and FAK of ASMCs were evaluated by western blotting and Ca influx of cells was measured by confocal laser microscope. Our data demonstrated that the proliferation, migration and MMP-2 expressions of ASMCs were inhibited by CDAE or CDE; the protein expressions of p38, Bcl-2 and FAK in ASMCs were substantially reduced by CDAE and CDE detected by western blotting or immunocytochemistry; also the increased calcium influx has been observed instantaneously after ASMCs were stimulated by CDAE or CDE. These findings suggested that Cortex Dictamni extracts might have inhibitory effects on ASMCs over-proliferation which could be one of the underline mechanisms for the therapy of asthma.