p38 MAPK信号通路调控二氧化硅诱导的人支气管上皮细胞上皮-间质转型  

p38 MAPK Signal Pathway Mediated Epithelial-mesenchymal Transition Induced by SiO_2 in Human Bronchial Epithelial Cells

作　　者：李飞凤[1] 周建华[1] 胡永斌[1] 高振芹[1] 邓征浩[1] 蒋海鹰[1] 

机构地区：[1]中南大学基础医学院,湖南长沙410013

出　　处：《工业卫生与职业病》2011年第2期69-73,共5页Industrial Health and Occupational Diseases

基　　金：国家自然科学基金(30700661);湖南自然科学基金(06JJ2098)

摘　　要：目的探讨p38 MAPK信号通路在二氧化硅(SiO2)诱导人支气管上皮细胞(human bronchialepithelial cells,HBE)上皮-间质转型(epithelial-mesenchymal transition,EMT)中的作用机制。方法采用MAPK活性检测试剂盒检测SiO2处理HBE细胞不同时间点p38活性改变;Western Blot检测矽尘诱导的HBE细胞E-cad、α-SMA和Vi mentin蛋白表达的改变。结果 SiO2作用于HBE细胞能诱导p38激酶活化,于30 min开始出现p38磷酸化水平增高,之后逐渐减弱;干预实验后免疫印迹结果显示,SB203580(30μmol/l)+SiO2(200μg/ml)干预组E-cad蛋白表达水平为SiO2(200μg/ml)处理组的(1.77±0.26)倍(P<0.05),α-SMA和Vi mentin表达减少,抑制率分别为34.67%和55.44%(P<0.05)。结论 SiO2在刺激HBE细胞发生EMT中能够激活p38;p38 MAPK信号通路调控SiO2的人支气管上皮细胞上皮-间质转型。Objective To investigate the role of p38 MAPK in SiO2 induced epithelial-mesenchymal transition（EMT）in human bronchial epithelial cells（HBE）in vitro.Methods The human bronchial epithelial cells were exposed to SiO2 and assessed the activation of p38 MAPK;the human bronchial epithelial cells were pretreated by SB203580 with different concentrations after 1 hour,and assessed alterations in the protein expression of E-cadherin,Vimentin and α-SMA.Results Western Blot showed that the activities of p38 MAPK at different time points induced by 200 μg/ml SiO2 significantly increased the phosphorylated p38 MAPK started from 30 min,and then gradually declined.When cells were pre-incubated with SB203580（30 μmol/L）＋SiO2（200 μg/ml）,the expression of E-cadherin increased（1.77±0.26） times of the SiO2（200 μg/ml）group（P0.05）.Meanwhile,α-SMA expression and Vimentin expression were suppressed,the inhibition rates were 34.67% and 55.44% respectively（P0.05）.Conclusions SiO2 could activate p38,p38 MAPK signal pathway could mediate epithelial-mesenchymal transition induced by SiO2 in human bronchial epithelial cells.

关 键 词：二氧化硅(SiO2) P38 MAPK 人支气管上皮细胞 上皮-间质转型 

分 类 号：R135[医药卫生—劳动卫生]