摘要
目的p38丝裂原活化蛋白激酶（p3SMAPK）在RCFs诱导BEAS-2B凋亡中的作用。方法10、20、40、80、160μg／cm^2RCF1、RCF2和RCF3诱导BEAS-2B细胞24h，用CCK-8法检测细胞存活率；20、40、100μg／cm^2RCF1、RCF2和RCF3诱导BEAS-2B细胞24h，用流式细胞仪检测细胞凋亡率的变化；40μg／cm^2RCF1、RCF2和RCF3诱导BEAS-2B细胞24h，Westernblot法检测磷酸化p38MAPK和Caspase-3蛋白的表达情况，上述检测均设阳性对照组、p38抑制剂SB203580干预组和正常组。结果随着染尘浓度增高，各浓度RCFs染尘组细胞存活率呈下降，细胞凋亡率增加。各浓度石棉＋sB组，20、40、80、160μg／cm^2RCF1＋sB组及40、80、160μg／cm^2RCF2＋SB组、RCF3＋SB组细胞存活率明显高于SB203580干预前，差异有统计学意义（P〈05）。与SB203580干预前比较，石棉＋sB组及20、40、100μg／cm^2RCFI＋SB组、RCF2＋SB组、RCF3＋SB组细胞凋亡率下降，差异有统计学意义（P〈0．05）。40μg／cm^2RCFs染尘组和阳性对照组磷酸化p38MAP／（蛋白表达增加，与正常组比较，差异有统计学意义（RO．05）。与正常组比较，40μg／cm^2。RCFs染尘组及阳性对照组Caspase-3蛋白表达增加，差异有统计学意义（P〈O．05）。石棉＋sB组及40μg／cm^2RCF1＋SB、RCF2＋SB、RCF3＋sB染尘组Caspase-3蛋白表达下调，与SB203580干预前比较，差异有统计学意义（P〈0．05）。结论p38MAPK在耐火纤维诱导的BEAS-2B凋亡中起重要作用。
Objective To investigate the role of p38 mitogen-aetivated protein kinases （MAPKs） in the apoptosis of human bronchial epithelial cells （BEAS-2B） induced by refractory ceramic fibers （RCFs）. Methods BEAS-2B cells were exposed to 10, 20, 40, 80, and 160 μg/cm^2 RCF1, RCF2, and RCF3 for 24 h, and the cell viability was measured by CCK-8 assay. BEAS-2B cells were exposed to 20, 40, and 100 μg/cm^2 RCF1, RCF2, and RCF3 for 24 h, and the cell apoptosis rate was measured by flow eytometry. BEA$-2B cells were exposed to 40 μg/cm^2 RCF1, RCF2, and RCF3, and the expression levels of phospho-p38 MAPK and caspase-3 were measured by Western blot. In each of the above treatments, the BEAS-2B cells were divided into positive control, p38 inhibitor SB203580 intervention, and normal groups. Results As the concentration of RCFs rose, the RCF exposure groups showed decreased cell viability and increased cell apoptosis rate. After SB203580 intervention, the intervention groups （all concentrations of asbestos ＋ SB, 20, 40, 80, and 160 μg/cm^2 RCFI＋SB, and 40, 80, and 160 pμg/cm^2 RCF2 and RCF3＋SB） had significantly increased cell viabilities （P〈0.05）, and the intervention groups （asbestos ＋ SB and 20, 40, and 100 μg/cm^2 RCF1, RCF2, and RCF3 ＋ SB） had significantly decreased cell apoptosis rates （P〈0.05）. Compared with the normal group, the RCF （40 μg/cm^2） exposure and positive control groups had significantly increased expression of phospho-p38 MAPK （,O〈0.05）, and the RCF （40 μg/cm^2） exposure group had significantly increased expression of caspase-3 （P〈0.05）. The intervention groups （asbestos ＋ SB and 40 μg/cm^2 RCF1, RCF2, and RCF3 ＋ SB） had significantly decreased expression of caspase-3 after SB203580 intervention. Conclusion p38 MAPKs play an important role in RCF- induced aoootosis of BEAS-2B cells.
出处
《中华劳动卫生职业病杂志》
CAS
CSCD
北大核心
2013年第5期347-350,共4页
Chinese Journal of Industrial Hygiene and Occupational Diseases
基金
浙江省自然科学基金（Y2090518）
浙江省卫生厅支撑学科建设基金（11-ZC02）
浙江省医学科学院青年基金（A70801S）
浙江省科技厅重大与高发疾病防治专项（2008C13029-2）
