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

目的：进一步探讨高压氧治疗脑缺血再灌注损伤，减轻神经元调亡朋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２０ｍｉｎ后再灌注３ｄ，并用０．１５ＭＰａ和０．２５ＭＰａ压力的高压氧治疗（６０ｍｉｎ／ｄ，连续３ｄ）后，应用免疫组化ＬＳＡＢ方法，观察高压氧对海巴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

EFFECT OF HYPERBARIC OXYGEN ON THE EXPRESSION OF PROTEINS Bcl-2 AND BAX IN THE GERBIL HIPPOCAMPUS CA1 FOLLOWING FOREBRAIN ISCHEMIA REPERFUSION

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.