Gao Xiaoqun, Chang Cheng, Duan Dongxiao, Ru Liqiang, Yin Guangfu
Department of Anatomy, Medical College of Zhengzhou University, Zhengzhou 450052, China.
J Huazhong Univ Sci Technolog Med Sci. 2006;26(1):17-20. doi: 10.1007/BF02828027.
In order to investigate the protective effect of hypoxic preconditioning on the cerebral ischemia-reperfusion injury, the expression of Bcl-2 and Bax was detected by using immunohistochemical staining after 3 h cerebral ischemia followed by 1, 6, 12, 24 and 48 h reperfusion respectively in rats treated with or without hypoxic preconditioning before cerebral ischemia. In addition, the apoptosis of neural cells and the behavioral scores for neurological functions recovery were evaluated by TUNEL staining and "crawling method", respectively. Compared with control group (cerebral ischemia-reperfusion without hypoxic preconditioning), the expression of Bcl-2 was significantly increased, but that of Bax decreased in the hypoxic preconditioning group (cerebral ischemia-reperfusion with hypoxic preconditioning), both P < 0.05. The pre-treatment with hypoxic preconditioning could reduce the apoptosis of neural cells and promote the neurological function recovery as compared to control group. It was suggested that hypoxic preconditioning may have protective effects on the cerebral ischemia-reperfusion injury by inhibiting the apoptosis of neural cells, increase the expression of Bcl-2 and decrease the expression of Bax.
为了研究缺氧预处理对脑缺血再灌注损伤的保护作用,在脑缺血前进行或不进行缺氧预处理的大鼠中,分别于脑缺血3小时后再灌注1、6、12、24和48小时,采用免疫组织化学染色检测Bcl-2和Bax的表达。此外,分别通过TUNEL染色和“爬行法”评估神经细胞凋亡和神经功能恢复的行为评分。与对照组(无缺氧预处理的脑缺血再灌注)相比,缺氧预处理组(有缺氧预处理的脑缺血再灌注)中Bcl-2的表达显著增加,而Bax的表达降低,两者P均<0.05。与对照组相比,缺氧预处理预处理可减少神经细胞凋亡并促进神经功能恢复。提示缺氧预处理可能通过抑制神经细胞凋亡、增加Bcl-2表达和降低Bax表达对脑缺血再灌注损伤具有保护作用。