OBJECTIVETo investigate the role of p38 mitogen-activated protein kinases (MAPKs) in the apoptosis of human bronchial epithelial cells (BEAS-2B) induced by refractory ceramic fibers (RCFs).

METHODSBEAS-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 cytometry. BEAS-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.

RESULTSAs 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)RCF1+SB, and 40, 80, and 160 µg/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 (P < 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.

CONCLUSIONp38 MAPKs play an important role in RCF-induced apoptosis of BEAS-2B cells.