粒细胞集落刺激因子对脑出血Bcl-2、Bax表达的影响

目的 通过探讨粒细胞集落刺激因子（G-CSF）作用于脑出血后凋亡调控基因的变化,评价G-CSF对脑出血细胞凋亡的影响机制.方法 将SD大鼠分为对照（Sham）组、脑出血（ICH）组、干预（CSF）组,每组各25只,后两组分为5个亚组,每亚组5只.采用自体尾动脉血造大鼠脑出血模型,TUNEL法及免疫组织化学法检测凋亡细胞及凋亡调控基因Bcl-2、Bax的表达.结果 ICH组凋亡细胞及Bcl-2、Bax较Sham组均增多（P〈0.01）;CSF组的凋亡细胞、Bax阳性细胞较ICH组均减少（P〈0.01）,Bcl-2阳性细胞增多（P〈0.01）;ICH组TUNEL细胞与Bax/Bcl-2表达呈负相关.结论 G-CSF可能通过控制凋亡调控基因Bax/Bcl-2的比率变化来调节脑出血血肿周围的细胞凋亡,为治疗脑出血提供可靠的分子靶点.

Effects of G-CSF on Expression of Bax and Bcl-2 after Intracerebral Hemorrhage in Rats

Objective To explore granulocyte colony stimulating factor（G-CSF）on apoptosis-regulation gene changes after cerebral hemorrhage, and the influence mechanism of evaluation of G-CSF on apoptosis in cerebral hemorrhage. Methods SD rats were divided into control group （Sham）, cerebral hemorrhage （ICH）group, and intervention（CSF）group,25 rats each group. In ICH and CSF groups,rats were divided into 5 subgroups with 5 rats each. Autologous artery blood was used to produce rat cerebral hemorrhage model,and the expression of apoptotic cells and apoptotic gene Bcl-2,Bax was examined by TUNEL and immunohistochemistry. Results In ICH group,the apoptotic cells and the Bcl-2, Bax expression were higher than in the Sham group（P〈0. 01）;apoptosis cells, Bax positive cells in CSF group were decreased（P〈0.01）, Bcl-2 positive cells were increased（P〈0.01）;in ICH group, the expression of Bax/Bcl-2 was negatively correlated with TUNEL cells. Conclusion G-CSF might change apoptosis regulatory gene Bax/Bcl-2 expression to regulate cerebral hemorrhage, and provide a molecular target for the treatment of cerebral hemorrhage.