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bcl-2及其同源基因bcl-xL的蛋白对DNA损伤诱导的细胞凋亡有保护作用，而另一有同源性的蛋白Bax是Bcl-2的拮抗物，促进细胞调亡。这些认识主要来自免疫系统的研究，但这组基因表达参与调节神经元生存与死亡的证据正在增加。方法：本研究通过鼠癫痫持续状态（SE）模型对海马细胞中这些基因的调节进行了检测。腹腔注射Bemegride诱导SD大鼠SE，摘记脑电图。以Northern杂交实验方法检测海马组织中bcl-2、bcl-XL和mRNA表达。结果：①中枢神经系统中有bcl-2、bcl-xL和baxmRNA表达；②SE后海马中bcl-2及bcl-xLmRNA升高，而baxmRNA略有降低。结论：海马bcl-2、bcl-xLmRNA增加及baXmRNA减少，表明bcl-2家族对SE后损伤的神经细胞起到调节作用。在其它涉及DNA损伤诱导调亡的神经疾病中也可能存在类似调节现象。
The protein of bcl-2 and its homologue bcl-xL has a protective effect on DNA damage-induced apoptosis, while another homologous protein Bax is an antagonist of Bcl-2 and promotes apoptosis. Much of this recognition comes from the study of the immune system, but evidence of the involvement of this group of genes in regulating neuronal survival and death is on the rise. Methods: In this study, the regulation of these genes in hippocampal cells was examined by the rat model of seizure status (SE). Intraperitoneal injection of Bemegride induced SD rats SE, EEG recorded. Northern blotting was used to detect the expression of bcl-2, bcl-XL and mRNA in hippocampus. Results: bcl-2, bcl-xL and bax mRNA were expressed in the central nervous system. B) Secretion of bcl-2 and bcl-xL mRNA in the hippocampus of SE rats was slightly lower than that in the control rats. CONCLUSION: Increased bcl-2, bcl-xL mRNA and decreased baXmRNA in the hippocampus indicate that the bcl-2 family regulates neuronal damage after SE. Similar regulation may exist in other neurological diseases that are involved in the DNA damage-induced apoptosis.