中文摘要：

目的探讨p38和ERK信号途径在紫外辐射B（UVB）导致细胞凋亡中的作用。方法以HaCat细胞为实验村料，“MTT”法观察细胞存活率：Hoechst33258染色后以荧光显微镜观察凋亡细胞的形态；免疫印迹观察此过程中的可能信号转导通路。结果UVB照射剂量不同，培养时间相同时，随剂量增加，HaCat细胞存活率逐渐减少；照射剂量相同，培养时间不同时．随时间延长．细胞存活率下降到最低值后开始恢复：UVB照射5min组的凋亡最高，并且5min照射组在照后培养12h时，凋亡率最高；UVB照射后p38及其下游的p53表达，而P44／42无改变。结论UVB照射，能引起HaCat细胞的生长抑制和凋亡且呈剂量依赖和时间依赖性：UVB导致细胞凋亡可能是通过p38信号途径，而不是ERK信号途径。

英文摘要：

Objective To explore the involvement of p38 and ERK signal transduction pathways in UVB-induced cell apoptosis. Methods HaCat cells were exposed to UVB irradiation for 1, 3, 5, 10, and 15 min, respectively, after which the cell survival was assessed using MTT assay, and the cell apoptosis observed under fluorescent microscope with Hoechst staining. Westem blotting was used to examine the possible signal transduction pathway involved in the cell apoptosis following the exposures. Results For the same incubation time following the exposure, the cell survival rate decreased gradually with the increase of UVB irradiation dose. At a fixed UVB irradiation dose, prolonged cell incubation following the exposure resulted in decreased cell survival rate, which, however, began to increase after the minimum rate was reached. At different UVB doses, cell exposure for 5 min caused the highest cell apoptosis rate, which peaked at 12 h during the post-irradiation incubation. The expressions of p38 and p53 were significantly decreased while p44/42 expression remained unchanged in the exposed cells. Condusion UVB irradiation can induce growth inhibition and apoptosis of HaCat cells in a dose- and time-dependent manner, and p38 pathway other than ERK pathway is probably involved in UVB-induced cell apoptosis.