缺氧预处理抑制新生鼠缺氧缺血性脑损伤细胞凋亡的观察

Observation of hypoxia preconditioning inhibiting the apoptosis in neonatal rats with hypoxic-ischemic brain damage

目的观察缺氧预处理(HPC)对新生大鼠缺氧缺血性脑损伤(HIBD)海马区Bcl-2和Bax表达的影响,探讨HPC对新生大鼠HIBD的保护机制。方法7日龄新生SD大鼠40只随机分为空白对照组、假手术组、HIBD组、HPC组。各组实验动物于缺氧缺血后24h处死,用免疫组织化学方法,检测脑组织海马区Bcl-2和Bax表达的变化。结果与空白对照组、假手术组相比,HIBD组和HPC组海马区Bcl-2蛋白和Bax蛋白表达明显增多(P<0.05);与HIBD组相比,HPC组海马区Bcl-2蛋白表达明显增多,Bax蛋白表达明显减少(P<0.05)。结论促进Bcl-2表达,抑制Bax表达,从而抑制细胞凋亡,是HPC对随后的HIBD的脑保护机制之一。

Objective To observe the effects of hypoxia preconditioning on the expression of Bcl-2 and Bax in hippocampus of the neonatal rats with hypoxia-ischemic brain damage, and discuss the neruoprotective mechanism of HPC to the HIBD of neonatal rats Methods Forty 7-day-old Sprague-Dawley rats were randomly divided into control group, sham operated group, hypoxia-ischemic brain damage group （HIBD group） and hypoxia preconditioning group（HPC group）. Immunohistochemistry staining was used to examine the expression of Bcl-2 and Bax in hippocampus. Results The amount of the positive cell of Bcl-2 and Bax of HIBD group and HPC group significantly increased compared with that of the control group and sham operated group; The amount of the positive cell of Bcl-2 of HPC group significantly increased and the amount of the positive cell of Bax of HPC group significantly decreased compared with that of HIBD group. Conclusion Hypoxia preconditioning protects cell from apoptosis by promoting the expression of bcl-2, reducing the expression of Bax and adjusting the ratio of Bcl-2/Bax, which would be one of the molecular mechanism of protective role in brain.