中文摘要：

目的探讨中波紫外线（UVB）诱导角质形成细胞凋亡机制。方法使用0、20、30、40、60、70、90mJ／cm^2 UVB辐射人角质形成细胞（HaCaT），辐射后0、1、2、3、4、6、24、48h收集细胞和上清。流式细胞仪检测细胞周期和凋亡；ELISA检测上清液中TNF-α水平；Western blot检测P38丝裂原活化蛋白激酶（P38MAPK）和磷酸化P38丝裂原活化蛋白激酶（p-P38MAPK）的表达。结果UVB（30mJ／cm^2）辐射后，HaCaT细胞分泌TNF-α逐渐增加，24h达高峰；P38抑制剂SB203580完全抑制TNF-α的分泌，部分阻止了细胞凋亡；以不同剂量UVB辐射HaCaT细胞，在30mJ／cm^2时p-P38MAPK表达量最高，且辐射后即可检测到p-P38MAPK的表达，1h时达高峰，以后逐渐下降，而P38MAPK表达量没有明显变化。结论紫外线可通过激活P38MAPK途经，促进TNF-α分泌来诱导角质形成细胞凋亡。

英文摘要：

Objective To examine the hypothesis that UVB irradiation promotes the secretion of inflammatory cytokines such as tumor necrosis factor α （TNF-α） from human keratinocyte （HaCaT） and induces cell apoptosis via P38 mitogen-activated protein kinase （MAPK） pathway. Methods HaCaT cells were divided into three groups： （ 1 ） control group, i.e. HaCaT without UVB irradiation; （2） HaCaT irradiated by UVB ; （ 3 ） HaCaT cultured together with SB203580 （ P38 MAPK inhibitor） and irradiated by UVB. Flow cytometry was used to test the apoptosis of the cells. ELISA was used to examine the concentration of TNF-α. In order to determine the signaling pathways induced by UVB, Western blot analysis was performed for P38 MAPK. Results P38 MAPK phosphorylation was detected immediately after UVB irradiation and peaked at 1 h. TNF-α secretion and cell apoptosis were strongly increased. SB203580 inhibited P38 MAPK activity, reduced the secretion of TNF-α, and prevented cell apoptosis. Conclusion P38 MAPK activation is one aspect of the signaling cascade that culminates in the secretion of TNF-α and contributes to cell apoptosis after UVB irradiation.