摘要
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。
bcl-2 and its homologue, bel-xL. encode membrane-associated protein that protects cell from DNA damage-inducd apoptosis, while Bax is Bcl-2 antagonist that promotes cel1 death. Although knowledge of the function of these genes' regulations has come largely from studying cell of the immune system, increasing evidence implicates these genes expreed in mediating neu7onaI survival or death. In the preselit study, we examined the regulation of these genes in hippeampus ce1l of status epi1epticus (SE) rat. Rat that injected Bemegride was induced status epilePticus. EEG was recorded. Northern blot eryriment showed the quantities exrend of bcl-2, bcl-x. and bax mRNA in hippocampus. bcl-2, bcl-xL and bax mRNA expreed in the central nervous system The hippocampus cel1s express upregu1ate bcl-2 and bel-xL mRNA, and downregUlate bax mRNA after status epilepticus. These data indicate that bcl-2, bel-XL mRNA expression increased and bax mRNA decreased in hippoCampus after status epi1epticus. It suggested that the protecti0n role 0f bcl-2 fam1y fot neurons injured after SE and perhaps other neurological diseases in which DNA damage induced apoptosis.
出处
《脑与神经疾病杂志》
1997年第3期141-143,共3页
Journal of Brain and Nervous Diseases
基金
国家自然科学基金!39330210
