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目的:研究电磁脉冲对恒河猴淋巴细胞的损伤作用及其机理,为其防护提供参考依据。方法:用本实验室建立的电磁脉冲发生源进行照射,照射场强为6×10~4V/m,在5min 内重复照射30次。脉宽为25～30 ns,单次脉冲前沿为20ns。用原位末端标记技术和麦格-姬姆萨染色检测凋亡细胞,用碱磷酶免疫组化技术检测 Bax和 Bcl-2凋亡相关蛋白的表达。结果:(1)上述场强照后1d,淋巴细胞凋亡即开始增多,照后3d 接近峰值,一直持续到照后14d,与对照(照前)值比较,在照后3、7、14d 淋巴细胞凋亡指数分别为对照值的2.2、2.5和2.2倍。(2)照射后外周血淋巴细胞数量也迅速减少,相同场强照射后3、7、14d 约为对照值的74%,77%79%。(3)照射后3d,淋巴细胞 Bax 蛋白即出现增加,7d 达到峰值,Bax 阳性的淋巴细胞约为对照值的3.1倍。而 Bcl-2蛋白照射后出现减少,于照后7d 降至最低,Bcl-2阳性的淋巴细胞约为对照值的36%。这些结果提示 Bax 能促进 EMP 诱发的淋巴细胞凋亡,而 Bcl-2则起抑制作用。结论:EMP 能够诱发恒河猴外周血淋巴细胞的大量凋亡,细胞凋亡可能是导致 EMP 照射后淋巴细胞数量迅速降低和免疫功能出现抑制的主要原因之一。Bax 和 Bcl-2在 EMP 诱发的淋巴细胞凋亡调控中起重要作用。
Objective: To study the effect and mechanism of electromagnetic pulse on the damage of rhesus monkey lymphocytes and provide a reference for its protection. Methods: The irradiation source of electromagnetic pulse was established in this laboratory. The irradiation field intensity was 6 × 10 ~ 4V / m, and the irradiation was repeated 30 times in 5 minutes. Pulse width of 25 ~ 30 ns, single pulse front of 20ns. Apoptotic cells were detected by in situ end labeling and Mage-Giemsa staining, and the expressions of Bax and Bcl-2 apoptosis-related proteins were detected by alkaline phosphatase immunohistochemistry. Results: (1) The apoptosis of lymphocytes began to increase on the 1st day after irradiation, and reached the peak on the 3rd day after irradiation, and continued to the 14th day after irradiation. Compared with the control Lymphocyte apoptosis index were 2.2, 2.5 and 2.2 times of the control. (2) The number of peripheral blood lymphocytes rapidly decreased after irradiation. The same field intensity was 74% and 77% 79% of the control at 3, 7 and 14 days after irradiation. (3) On the 3rd day after irradiation, Bax protein in lymphocytes increased, reaching the peak on the 7th day. The number of Bax-positive lymphocytes was about 3.1 times that of the control. However, Bcl-2 protein decreased after irradiation, and reached the lowest level at 7 days after irradiation. The Bcl-2-positive lymphocytes were about 36% of the control. These results suggest that Bax can promote EMP-induced lymphocyte apoptosis, while Bcl-2 plays an inhibitory role. CONCLUSION: EMP can induce a large number of apoptosis in peripheral blood lymphocytes of Rhesus monkeys. Apoptosis may be one of the main causes of the rapid decrease of lymphocyte number and suppression of immune function after EMP irradiation. Bax and Bcl-2 play an important role in the regulation of EMP-induced lymphocyte apoptosis.