高压氧对脑缺血再灌注海马神经元Bcl-2和Bax蛋白表达的影响

EFFECT OF HYPERBARIC OXYGEN ON THE EXPRESSION OF PROTEINS Bcl-2 AND BAX IN THE GERBIL HIPPOCAMPUS CA 1 FOLLOWING FOREBRAIN ISCHEMIA REPERFUSION

目的 :进一步探讨高压氧治疗脑缺血再灌注损伤 ,减轻神经元凋亡从而发挥保护作用的机理。方法 :采用“双侧颈总动脉阻断法”前脑缺血模型 ,对沙土鼠前脑缺血 2 0min后再灌注 3d ,并用 0 .15MPa和 0 .2 5MPa压力的高压氧治疗 (6 0min/d ,连续 3d)后 ,应用免疫组化LSAB方法 ,观察高压氧对海马CA1,区神经元凋亡相关基因bcl 2和bax的蛋白表达的影响。结果 :沙土鼠脑缺血再灌注 3d组海马CA1区大量神经元表达Bax蛋白 ,并且神经元发生凋亡 ,未见神经元表达Bcl 2蛋白 ;高压氧治疗组则大量神经元表达Bcl- 2蛋白 ,并且 0 .2 5MPa高压氧治疗组比0 .15MPa高压氧治疗组变化更显著 ,而各组表达Bax蛋白的神经元数目无明显变化 ,但高压氧治疗组Bax蛋白阳性的神经元形态正常。结论 :HBO暴露可诱导大量神经元表达Bcl- 2蛋白 ,对Bax蛋白表达则无明显作用 ,使Bcl 2和Bax蛋白表达的比值增高 ,从而起到保护神经元的作用 。

Aim: To study the mechanisms of how hyperbaric oxygen treatment ( HBOT ) reduced neuronal apoptosis following forebrain ischemia reperfusion. Methods: Changes of the expression of protein Bcl 2 or Bax were observed in CA 1 region of gerbil hippocampus following HBOT on ischemia reperfusion 3 days using the method of labelled streptavidin biotin (LSAB)immunohistochemistry stai ning. For this purpose gerbils were exposed to the 0.15 MPa and 0.25MPa HBO 60min every day for 3 successive days. Results: The expression of protein Bcl 2 in hippocampus CA 1 was significantly increased in HBOT groups ( P <0.01), and changes in 0.25 MPa groups were greater than those in 0.15MPa groups ( P <0.01). The expression of protein Bax in hippocampus CA 1 was not changed significantly in HBOT groups. Conclusion: HBO can induce the expression of Bcl 2, which is the mechanism of neuronal protecting effect of HBOT.