国际麻醉学与复苏杂志   2015, Issue (3): 7-7
    
高压氧治疗对阿尔茨海默病大鼠海马内神经元凋亡及p38MAPK表达的影响
赵柏松1()
1.广州市妇女儿童医疗中心麻醉科
The effect of hyperbaric oxygen treatment on hippocampal the neuron apoptotic and the expression of p38MAPK in alzheimer disease rat model
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摘要：

目的 评价高压氧治疗对阿尔茨海默病（AD）大鼠海马内神经元凋亡及p38MAPK表达的影响。方法 18只雄性SD大鼠，体重260～290g，采用随机数字表法将其分为3组（n=6）：生理盐水组（NS组）海马区注射生理盐水；阿尔茨海默病组（AD组）海马区注射Aβ1-40；高压氧组（HBO组）海马区注射Aβ1-40，并于术后1~7d行每天一次的高压氧治疗。应用脑立体定位仪于大鼠海马区注射Aβ1-40制备AD模型。于术前1d和术后21d行水迷宫行为学测试。于术后21d水迷宫行为学测试结束后处死大鼠，采用HE染色海马组织病理结构，TUNEL法标记检测凋亡细胞，Western-bolt法测定海马内p38MAPK蛋白磷酸化水平。结果 术前1d相比，术后21d时AD组和HBO组大鼠上台前路程和逃避潜伏期增加(P<0.05)；于术后21d时，与NS组相比，AD组和HBO组大鼠上台前路程和逃避潜伏期增加，且海马内神经元细胞凋亡率和p38MAPK的磷酸化水平均升高(P<0.05)。 结论 高压氧治疗可有效缓解AD大鼠认知功能障碍，且能够抑制海马内神经元凋亡，其机制与降低p38MAPK的磷酸化水平有关。
关键词： 认知障碍；高压氧；凋亡；磷酸化p38MAPK；海马
Abstract:

Objective To investigate the effect of hyperbaric oxygen treatment on hippocampal the neuron apoptotic and the expression of p38MAPK in alzheimer disease rat model. Methods Eighteen healthy male SD rats weighing 260~290 g were randomly divided into 3 groups (n=6) normal saline group (group NS), alzheimer disease group (group AD) and hyperbaric oxygen treatment group (group HBO). The animal model of cognitive dysfunction was established after Aβ1-40 was injected into hippocampus in rats of group AD and group HBO, and the same volume normal saline but not Aβ1-40 was injected in group NS. The rats in group HBO received hyperbaric oxygen treatment daily for 7d, 1 d after AD models were established whereas rats in group S and NP placed in hyperbaric chamber 100 min and did not receive any treatment. Morris waters-maze test was performed on 1 day before injection-surgery and 21th day after injection-surgery each group.The animals were sacrificed after behavior test the last time, the hippocampus then were removed to detect the apoptosis of hippocampal neurons was evaluated by TUNEL staining, and the expression of p-p38MAPK were observed by Western Bolt. Result Compared with1 day before injection-surgery，the swimming distance and escape latent period were significantly longer in group AD and group HBO on the 21d day after surgery (P<0.05). Compared with group NS, the swimming distance and escape latent period were significantly longer in group AD on the 21d day after surgery, the neuron apoptotic rate and the expression of p-p38MAPK in hippocampus was significantly enhanced in group AD on the 21d day after surgery (P<0.05). Compared with group AD, the swimming distance and escape latent period were significantly shorter, the neuron apoptotic rate and the expression of p-p38MAPK in hippocampus was significantly down-regulated in group AD on the 21d day after surgery (P<0.05). Conclusion HBO treatment can alleviate the cognitive dysfunction of AD and decease the apoptosis induced by Aβ in rats, and the mechanism is related to inhibiting p-p38MAPK .
Key words: cognitive dysfunction; hyperbaric oxygen ; apoptosis；p-p38MAPK；hippocampus