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目的 通过研究照射剂量与垂体瘤细胞凋亡的关系,探讨射线诱导调亡的机制,为临床上进一步实行个体化治疗提供依据。方法 对5例垂体瘤标本行垂体瘤的细胞培养,分别设置对照组、5Gy、10Gy、15Gy、20Gy、25Gy组,模拟X-刀剂量。采用直线加速器(美国Varian600C)6MV的X射线,射野为10cm×10cm;深度为3cm,照射完毕后,常规培养24～48小时后进行下一步检测。采用流式细胞仪检测凋亡细胞和细胞免疫组化法:P53和Bcl-2基因的表达。结果 随着照射剂量增加,正常存活细胞逐渐减少,而调亡和坏死细胞数逐渐增加,照射10～15Gy时细胞调亡率最高,剂量进 一步增加,细胞凋亡率也不再增加。凋亡组内P53基因表达高于对照组。结论 射线诱导的细胞凋亡是P53基因依赖性凋亡。Bcl-2基因表达低于对照组,说明它的过度表达抑制细胞凋亡。
OBJECTIVE: To study the mechanism of radiation-induced apoptosis by studying the relationship between radiation dose and apoptosis of pituitary tumor cells, and provide the basis for further clinical practice. Methods Five pituitary tumor specimens were cultured in vitro. The control group, 5 Gy, 10 Gy, 15 Gy, 20 Gy and 25 Gy groups were set up to simulate the X-knife dose. Using a linear accelerator (American Varian600C) 6MV X-ray, the radiation field of 10cm × 10cm; depth of 3cm, after irradiation, conventional culture 24-48 hours after the next test. Flow cytometry was used to detect apoptotic cells and cellular immunohistochemistry: expression of P53 and Bcl-2 genes. Results With the increase of radiation dose, the number of surviving cells decreased gradually and the number of apoptotic and necrotic cells increased gradually. The highest rate of apoptosis and the further increase of apoptosis rate were observed at 10 ~ 15 Gy irradiation, and the rate of apoptosis was no longer increased. P53 gene expression in apoptotic group was higher than that in control group. Conclusions Radiation-induced apoptosis is P53-dependent apoptosis. Bcl-2 gene expression is lower than the control group, indicating that its overexpression inhibits apoptosis.