丝裂原活化蛋白激酶信号转导通路在电磁辐射诱导PC12细胞凋亡中的作用

Effect of mitogen activated protein kinase signal transduction on apoptosis of PC12 cells induced by electromagnetic exposure

目的探讨丝裂原活化蛋白激酶（MAPK）信号转导系统的差别激活与电磁辐射诱导PC12细胞凋亡的关系。方法经MAPK特异性抑制剂SB203580、U0126预处理的PC12细胞接受65mW／cm^2电磁波辐照20min，在辐照后3、24h2个观察时相点，采用蛋白质免疫印迹方法检测ERK1／2、JNK、P38MAPK蛋白质磷酸化水平，采用Annexine-V-FITC标记流式细胞仪检测PC12细胞凋亡率。结果电磁辐射后，PC12细胞ERK1／2的激活可以被U0126明显抑制，而SB203580对其无抑制作用。U0126和SB203580对辐照后JNK的活性无明显影响。SB203580可以明显抑制P38MAPK的激活，而U0126对P38MAPK激活的抑制作用不明显。SB203580可以明显减轻电磁辐射诱导的PC12细胞凋亡，而U0126预处理对细胞凋亡无明显影响。结论电磁辐射诱导PC12细胞凋亡主要通过P38MAPK信号通路的激活调控，而ERK通路对电磁辐射诱导的细胞凋亡无明显影响，JNK可能对辐照后早期的细胞凋亡有一定促进作用。

Objective To observe the effect of mitogen activated protein kinase （MAPK） signal transduction system on the apoptosis induced by electromagnetic exposure in PC12 cells. Methods After pretreated by SB203580 alone or together with U0126 ,PC 12 cells were exposed to 65 mW/cm^2 electromagnetic wave for 20 rain. The phosphorylations of ERK1/2,JNK and P38 MAPK were tested by Western-blot at 3 h and 24 h after electromagnetic exposure. The apoptosis of PC12 cells were detected by Annexine-V-FITC flow cytometry. Results U0126,but not SB203580 could inhibit the activation of ERK1/2 induced by electromagnetic exposure. U0126 and SB203580 had no effects on the activation of JNK. SB203580 could inhibit the activation of P38 MAPK significantly. But U0126 had no such effect on the activation of P38 MAPK. After pretreated by SB203580 alone or together with U0126,the apoptosis of PC12 cells decreased. But the pretreatment by U0126 alone had no influence on the apoptosis of PC12 cells. Conclusion The P38 MAPK signal transduction modulate the apoptosis of PC12 cells induced by electromagnetic exposure. ERK signal transduction has no effect on the apoptosis of PC12 cells. JNK signal transduction may promote the apoptosis of PC 12 cells in the early stage after electromagnetic exposure.