高压氧对缺氧缺血新生大鼠脑组织神经可塑性相关蛋白的影响

目的研究高压氧(HBO)对缺氧缺血新生大鼠脑组织神经相关蛋白(GAP-43)和神经生长抑制因子(Nogo-A)的影响,探讨HBO对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用及机制。方法7日龄Wistar大鼠24只随机分为3组:正常对照组(CON组),HIBD组和HBO组,每组各8只,HBO组于缺氧缺血1h后行HBO处理,每日1次,连续7d。各组分别于17日龄时处死取材。苏木素-伊红(HE)染色观察脑组织病理改变,免疫组织化学方法检测3组大鼠大脑皮层GAP-43蛋白和Nogo-A表达。结果HBO组病理改变较HIBD组减轻。GAP-43表达:平均灰度值HIBD组较正常对照组明显降低(P<0.05),HBO组较HIBD组明显降低(P<0.05)。Nogo-A表达:平均灰度值HIBD组较正常对照组降低(P<0.05),HBO组较HIBD组明显增加(P<0.05)。结论HBO治疗可以通过增加缺氧缺血新生大鼠脑组织GAP-43蛋白和降低Nogo-A的表达,发挥其对脑损伤的保护作用。

Influence of HBO on relative proteins with heural plasticity in brain tissue of HIBD rat

Objective To probe into the protecting effect and mechanism of hyperbaric oxygen(HBO)therapy on neonatal rats with hypoxic-ischemic brain damage by studying the influence of HBO on nerve growth associated protein GAP-43 and nerve growth inhibitor Nogo-A in brain tissue of neonatal rat.Methods A total of 24 7 d-Wistar rats were randomly divided into normal control(CON)group,HIBD group and HBO group(n=8 in each group);HBO therapy was carried out for HBO group cases at 1 h after hypoxic-ischemic,once a day and lasting 7 d.Cases in each group were executed and the materials were drew from the brain at 17-day-old.The pathological changes in brain were observed by optical microscope and the expression of GAP-43 and Nogo-A in cerebral cortex was examined with immunohistochemical staining and image quantitative analysis.Results The pathological changes of HBO group cases were relieved compared with HIBD group cases.The average gray scale value of HIBD group cases was lower than that of CON group cases(P<0.05),and the average gray scale value of HBO group cases was lower than that of HIBD group cases(P<0.05).The expression of Nogo-A:the average gray scale value of HIBD group cases was decreased compared with HIBD group cases(P<0.05),and the average gray scale value of HBO group cases was increased compared with HIBD group cases(P<0.05).Conclusion HBO therapy can protect the brain tissue by increasing the expression of GAP-43 and reduce the expression of Nogo-A in neonatal rats with hypoxic-ischemic brain damage.