UV通过p38MAPK促进大鼠胶质瘤C6细胞凋亡

目的：探讨p38MAPK在紫外线损伤刺激细胞中的特异性信号转导作用。方法：流式细胞仪检测紫外线照射30min后1，2及4h的C6细胞周期变化和是否有凋亡发生；应用免疫细胞化学技术观察紫外线刺激前后p38MAPK在C6细胞中的表达强度和分布特征。结果：细胞周期结果显示1，2和4h后C1期细胞数分数各增多0．12，0．21和0．19，而S期细胞数分数减少0．10，0．14和0．15；各组的凋亡率分别是12％，49％和34％；未受刺激的细胞中，p38MAPK在胞质和胞核表达较弱；紫外线损伤作用2h后，细胞核区的染色强度即明显增强，而胞质区域的染色强度相对降低。结论：C6细胞受紫外线损伤后可通过p38MAPK通路发生凋亡。

Rat glioma C6 cell apoptosis induced by UV radiation via p38-MAPK

AIM: To study the signal transduction of p38 mitogen activated protein kinase in rat glioma C6 cells after the stimulation of UV radiation. METHODS: Flow cytometry was applied to measure the fraction number changes in the cell cycle phase and to detect whether UV could induce apoptosis of C6 cells. The level and distribution of p38MAPK expression was examined by immunocytochemical method both before and after the UV radiation. RESULTS: Flow cytometry indicated that the numbers of G1 phase fraction of 1,2 and 4h groups accumulated by 0.12, 0.21 and 0.19 respectively and those of S phase fraction reduced by 0.10, 0.14 and 0.15 respectively and their apoptosis rates were 12%, 49% and 34% respectively in the UV treated groups. 2h after the UV radiation, p38MAPK was strongly expressed and distributed mainly in the nucleus of C6 cells while for the untreated C6 cells, p38MAPK was weakly dispersed in the whole cell. CONCLUSION: Apoptosis of rat glioma C6 cells is induced by UV radiation via p38MAPK.