粒细胞集落刺激因子与血管性痴呆大鼠海马凋亡相关蛋白

背景：研究表明粒细胞集落刺激因子在保护神经元免受各种因素所致的神经元变性和死亡中发挥重要作用。 目的：观察粒细胞集落刺激因子对血管性痴呆大鼠海马组织神经细胞凋亡及Bcl-2、Bax蛋白表达的影响。 方法：采用永久性双侧颈总动脉结扎法建立SD大鼠血管性痴呆模型，以未进行血管结扎的大鼠作为假手术组。造模成功后，治疗组大鼠每日皮下注射粒细胞集落刺激因子50 μg/kg，假手术组和模型组注射等量的生理盐水。分别于造模后7，14，28 d取大鼠海马组织用于检测。 结果与结论：Morris水迷宫结果显示，模型组大鼠逃避潜伏期明显延长(P < 0.01)，而治疗组各时间点大鼠逃避潜伏期较模型组缩短(P < 0.01)；TUNEL及免疫组织化学结果显示，与模型组比较，治疗组各时间点大鼠海马TUNEL及Bax阳性细胞吸光度值明显减小(P < 0.01)，Bcl-2阳性细胞吸光度值明显增加(P < 0.01)。说明粒细胞集落刺激因子可提高血管性痴呆大鼠海马Bcl-2蛋白的表达，抑制Bax蛋白的表达，减少神经细胞凋亡，改善大鼠的学习记忆功能。

Effect of granulocyte colony-stimulating factor on the expression of hippocampal apoptosis-related protein in rats with vascular dementia

BACKGROUND:Studies have demonstrated that granulocyte colony-stimulating factor plays an important role in protecting neurons from neuronal degeneration and death caused by a variety of factors. OBJECTIVE:To investigate the effect of granulocyte colony-stimulating factor on hippocampal neuronal cell apoptosis and Bcl-2 and Bax protein expression in rats with vascular dementia. METHODS:The permanent bilateral common carotid artery ligation method was used to establish the Sprague-Dawley rat vascular dementia models. Rats with no vascular ligation were included in the sham-operation group. Rats in the treatment group were subcutaneously injected with 50 μg/kg granulocyte colony-stimulating factor daily, rats in the sham-operation group and model group were injected with normal saline. At 7, 14 and 28 days after modeling, rat hippocampus was used for detection. RESULTS AND CONCLUSION:Morris water maze results showed that the escape latency of the rats in the model group was significantly prolonged (P < 0.01), and the escape latency at different time points in the treatment group was shorter than that in the model group (P < 0.01). TUNEL and immunohistochemistry results showed that, compared with the control group, rat hippocampal TUNEL and Bax positive cell number in the treatment group were significantly reduced (P < 0.01), and the number of Bcl-2 positive cells was significantly increased (P < 0.01). Granulocyte colony-stimulating factor can up-regulate Bcl-2 protein expression in the hippocampus of vascular dementia rats, down-regulate Bax protein expression, reduce neuronal apoptosis and improve the learning and memory abilities of rats.