高压氧对急性一氧化碳中毒迟发性脑病大鼠学习记忆能力及脑组织髓鞘碱性蛋白的影响

Effects of hyperbaric oxygen on learning and memory ability and myelin basic proteins in brain tissue after carbon monoxide poisoning

目的观察高压氧（HBO）对急性一氧化碳中毒（COP）迟发性脑病大鼠学习记忆及脑组织髓鞘碱性蛋白（MBP）表达的影响。方法选取雄性SD大鼠45只，经Morris水迷宫筛选后，分为正常对照组（NC组）11只、急性一氧化碳中毒组（COP组）17只和急性一氧化碳中毒高压氧治疗组（／-IB．O组）17只。COP组和HBO组采用分次腹腔注射CO气体法建立大鼠急性COP迟发性脑病模型，NC组采用相同方法腹腔注射等量空气。造模成功后，HBO组大鼠进行HBO治疗，NC组及COP组均给予常压饲养。与造模成功后第1天至造模成功后第21天对3组大鼠进行水迷宫测试，观察其学习记忆能力的变化情况，并于造模成功后第21天检测3组大鼠脑组织中MBP的表达情况。结果造模后21d内，COP组迟发性脑病发病9只（64．3％），HBO组发病4只（26．7％），2组间差异有统计学意义（P〈0．05）。HBO组大鼠平均逃避潜伏期为（6．20±1．98）s，与COP组的（10．61±4．82）S比较，差异有统计学意义（P〈0．05）。造模成功后第21天，COP组和HBO组大鼠脑组织MBP的表达均低于NC组（P〈0．05）；COP组大鼠脑组织MBP的表达低于HBO组（P〈0．05）。3组大鼠脑组织灰度值比较，NC组显著优于COP组和HBO组（P〈0．05），而HBO组亦显著优于COP组（P〈0．05）。结论HBO治疗能改善急性COP迟发性脑病大鼠学习记忆能力，减轻脑组织脱髓鞘损伤。

Objective To observe the effects of hyperbaric oxygen （HBO） on learning and memory ability and on the level of myelin basic protein （MBP） in the brain tissue of rats with delayed neurological sequelae （DNS） after acute carbon monoxide poisoning （COP）. Methods Forty-eight male SD rats had their cognitive performance assessed with the Morris water maze. After basic training with the Morris water maze and screening, the rats were ran- domly divided into a normal control （NC） group （n=ll）, a COP group （n =17） and an HBO group （n = 17）. Pure CO gas was injected intraperitoneally to establish acute COP in the latter two groups. The NC group received a similar injection of air. The HBO group was given HBO therapy. The rats in each group were tested for changes in their learning and memory abilities using the Morris water maze. On the 21st day after the treatment, paraffin tissue sections of the rats＇ brains were subjected to immunohistochemical （IHC） examination and Western blotting （WB） was used to detect any expression of MBP in the brain tissue. Results After 21 days, morbidity among the COP group was 64.3% , while it was 26.7% in the HBO group, a significant difference. The average maze escape latency in the COP group was significantly longer than in the HBO group. IHC staining and Western blotting showed that MBP in the hippocampal tissue of the COP group was significantly lower than that in the HBO group. In gray scale comparisons of the rats＇ brain tissue, that from the NC group was significantly better than that from the COP and HBO groups, but that from the HBO group was significantly better than that from the COP group. Conclusion HBO can effectively reduce DNS after acute COP, mitigate the severity of DNS, reduce demyelination of brain tissue and thus play an important role in protecting brain cells.