论文部分内容阅读
目的 Epithelial-mesenchymal transition(EMT)plays a criticalrole in airway repair and remodeling in many respiratory diseases such as asthma and pulmonary fibrosis.The flavone aglycone,diosmetin,possesses anti-remodelingactivity in a murine model of chronic asthma,but little is known about itseffects on EMT.Herein,we investigated whether diosmetin inhibits transforminggrowth factor-β1(TGF-β1)-induced EMT with an emphasis on oxidative stress modulation in human bronchial epithelial(HBE)cells.方法 HBE cells were incubated with 10 ng/ml TGF-β1 alone or along with diosmetin for indicated time.The level of reactive oxygen species(ROS)was measured following co-incubated with dichlorodihydrofluorescein diacetate assay by FACScan and immunofluorescent assay.The protein expression such as NADPH oxidase 4(NOX4),superoxide dismutase(SOD),catalase,Akt,Erk,p38 were assessed by Western blot analysis.结果 TGF-β1 promoted EMT in HBE cells and generation of ROS.Diosmetin significantly suppressed TGF-β1-induced increases of cell migration and alteration of E-cadherin,N-cadherin and α-smooth muscle actin expression.In addition,diosmetin prevented TGF-β1-induced intracellular ROS generation,down-regulated NOX4,SOD and catalase expression.Furthermore,diosmetin remarkably inhibited activation of phosphoinositide 3-kinase(PI3K)/Akt and mitogen activated protein kinase(MAPK)signaling pathways induced by TGF-β1 in HBE cells.结论 Our results demonstrated for the first time that diosmetin alleviates TGF-β1-induced EMT via inhibiting ROS generation as well as inactivating PI3K/Akt and MAPK pathways.The findings revealed a new profile of diosmetin in remitting airway remodeling and fibrogenesis.