中文摘要：

目的：探讨选择性周期素依赖性蛋白激酶抑制剂Olomoucine对局灶性脑缺血后星形胶质细胞增殖及胶质疤痕形成的抑制作用。方法：将72只SD大鼠随机分为假手术组12只、模型组27只和干预组33只。3组均手术暴露颅骨，模型组和干预组建立光化学法诱导大鼠局灶性脑缺血模型，之后干预组腹腔注射Olomoucine，分别将3组大鼠于处理后3、7、30d处死，应用免疫组织化学法检测梗死灶周围胶质纤维酸性蛋白（GFAP）的表达；Western blot法观察损伤侧皮质GFAP、增殖细胞核抗原（PCNA）、周期素蛋白A（CyclinA）和周期素蛋白B1（CyclinB1）的表达。结果：缺血后各组梗死灶边缘区GFAP表达明显增强，缺血后7和30d模型组GFAP表达明显强于干预组（P〈0．05），并且7和30d对照组缺血边缘区可见胶质疤痕形成，尤以30d最为明显；GFAP、PCNA、CyclinA和CyclinB蛋白的表达，模型组明显高于干预组（P〈0．05）。结论：Olomoucine可部分抑制胶质细胞的活化增殖及疤痕的形成。该结果提示调控细胞周期可能是治疗脑缺血新的方向。

英文摘要：

Objective： The effect of a cell cycle inhibitor, olomoucine, on astrocytic proliferation was studied by measuring astrocytic proliferation and scar formation after focal cerebral ischemia in rats. Methods： An ischemic rat model was generated by photochemistry method. The expression of glial fibrillary acidic protein （GFAP） was studied by immunofluoreseence. Protein levels for GFAP, proliferation cell nuclear antigen （PCNA）, cyclin A and cyclin B1 were investigated by Western blot at days 3, 7 and 30 after operation. Results： Olomoucine significantly reduced the expression of GFAP. In parallel study, glial scar tissue was observed near infarct regions in control rats at 7 and 30 days, and its density of scar formation was significantly greater at 30 days than at 7 days. Olomoucine significantly inhibited scar formation. Western blot showed increased protein levels for GFAP, PCNA, CyclinA and CyclinB1 in control rats, while the up-regulation of the proteins above was inhibited by olomoucine. Conclusion： The study suggested that olomoucine could significantly inhibit activation, proliferation and scar formation of astrocytes. Regulating cell cycles may provide a new method for treating cerebral ischemia.