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目的:研究Bcl-2对缺血性脑损伤保护作用的机制。方法:采用侧脑室微量注射、免疫组织化学法和焦油紫染色法在大鼠大脑中动脉栓塞模型上,观察Bcl-2反义寡脱氧核苷酸(antisense oligodeoxynucleotides,antisense ODNs)对DNA修复基因ERCC1(excisionrepair cross-complementing group 1)表达的影响。结果:antisense ODNs能抑制缺血周边Ⅰ区Bcl-2的表达(P<0.01),加重该区域脑缺血损伤。同时,ERCC1的表达也有下降的趋势(P=0.087),而且,在Bcl-2表达的区域,也有ERCC1的表达。结论:Bcl-2对缺血神经元的保护作用与调节脑细胞内源性的DNA修复有关。
Objective: To study the mechanism of the protective effect of Bcl-2 on ischemic brain injury. Methods: The model of middle cerebral artery occlusion (MCAO) was induced by intracerebroventricular microinjection, immunohistochemistry and tar violet staining. The effect of antisense oligodeoxynucleotides (antisense ODNs) against ERCC1 (excisionrepair cross-complementing group 1) expression. Results: Antisense ODNs could inhibit the expression of Bcl-2 in the peripheral area of ischemic area (P <0.01), aggravating the ischemic injury in this area. Meanwhile, the expression of ERCC1 also showed a decreasing trend (P = 0.087), and the expression of ERCC1 was also observed in the area of Bcl-2 expression. Conclusion: The protective effect of Bcl-2 on ischemic neurons is related to the regulation of endogenous DNA repair in brain cells.