摘要
目的 探讨低氧预适应 (8%O2 ,3h)对大鼠大脑中动脉缺血 3h再灌注后不同时间脑梗死体积、神经细胞凋亡及Bcl 2、BaxmRNA及其蛋白表达的影响。方法 低氧预适应后 12h制作脑缺血再灌注模型。在大鼠大脑中动脉缺血 3h再灌注后不同时间进行脑梗死体积测定 (TTC)和原位细胞凋亡检测 (TUNEL) ,通过Northernblot检测脑组织中Bcl 2、BaxmRNA的表达以及免疫组化检测Bcl 2、Bax蛋白的表达。结果 低氧预适应组的脑梗死体积、神经细胞凋亡、Bax的表达较缺血再灌注组明显减少 ;Bcl 2的表达明显增高。结论 低氧预适应可减少大脑中动脉缺血 3h再灌注后梗死体积 ,增强Bcl 2及减少Bax的表达 ,抑制神经细胞的凋亡可能是其脑保护机制之一。
Objective To study the effect of hypoxic preconditioning in 8 % O_2 for 3 h on the rat brain infarct volume, neural cells apoptosis, and the expression of mRNA and protein of Bcl-2 and Bax in rat cerebral ischemia/reperfusion. Methods Rats were subjected to hypoxic preconditioning for 12 h to develop cerebral ischemia-reperfusion model. After ischemia for 3 h and 1 h, 6 h, 12 h, 24 h and 48 h following reperfusion in middle cerebral artery, the sections of rat brain were applied for brain infarct volume by TTC, neural apoptosis by TUNEL staining, the protein expression of Bcl-2 and Bax by immunohistochemistry, and the mRNA expression of Bcl-2 and Bax by Northern blot. Results The brain infarct volume, neural apoptosis, the expression of Bax in the hypoxic preconditioning group were significantly decreased, and the expression of Bcl-2 was significantly increased as compared with the control group. Conclusion One of the mechanisms of brain protection by hypoxic preconditioning may be contributed to the decrease of the brain infarct volume, neural apoptosis, and the expression of Bax and the increase of the expression of Bcl-2.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2004年第5期546-549,F003,共5页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
