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目的探究高压氧改善一氧化碳中毒后迟发性脑病大鼠学习记忆能力可能的机制。方法选择雄性SD(Sprague Dawley)大鼠32只,鼠龄3个月,体质量(220±10)g。随机数字法分为对照组(NC组)、一氧化碳中毒组(COP组)、一氧化碳中毒后迟发性脑病组(DNS组)、高压氧治疗组(HBO组),每组8只。利用腹腔注射空气建立NC组模型;利用腹腔注射CO气体、Morris水迷宫、动物高压氧舱建立大鼠COP组、DNS组及HBO组模型。通过Morris水迷宫采集各组大鼠平均逃逸潜伏期、平台穿越次数、平台象限游泳距离等参数评估其学习记忆能力,通过流式细胞仪检测海马神经细胞凋亡程度;通过免疫组织化学染色法及蛋白免疫印迹法检测各组大鼠海马组织c-Jun蛋白表达情况,并将c-Jun蛋白表达情况与各参数进行双变量相关分析。结果与NC组相比,COP组、DNS组、HBO组学习记忆能力下降;HBO组学习记忆能力较DNS组提高(P<0.05),与NC组相比,COP组、DNS组、HBO组海马神经细胞凋亡程度上升;HBO组海马神经细胞凋亡程度较DNS组下降。与NC组相比,COP组、DNS组、HBO组大鼠海马组织中c-Jun蛋白表达升高(P<0.05);HBO组大鼠海马组织中c-Jun蛋白表达较DNS组下降(P<0.05)。双变量相关分析结果显示,COP组、DNS组、HBO组中c-Jun蛋白表达与平均逃逸潜伏期呈正相关,与平台穿越次数、平台象限游泳距离呈负相关。结论一氧化碳暴露,尤其是一氧化碳中毒后迟发性脑病的发生可以引起c-Jun蛋白过度表达,导致学习记忆能力下降。高压氧治疗能够改善一氧化碳中毒后迟发性脑病大鼠学习记忆能力,其机制可能与调控海马组织c-Jun蛋白表达相关。
Objective To explore the possible mechanism of hyperbaric oxygen to ameliorate the learning and memory ability of rats with delayed encephalopathy after carbon monoxide poisoning. Methods Thirty - two male Sprague - Dawley rats were selected and their age was 3 months. The body weight was (220 ± 10) g. Random number method was divided into control group (NC group), carbon monoxide poisoning group (COP group), carbon monoxide poisoning delayed encephalopathy group (DNS group) and hyperbaric oxygen therapy group (HBO group). The model of NC group was established by intraperitoneal injection of air. The models of COP, DNS and HBO groups were established by intraperitoneal injection of CO gas, Morris water maze and animal hyperbaric chamber. Morris water maze test was used to evaluate the learning and memory abilities of rats in each group, such as the average escape latency, the number of platform traverses and the swimming distance of platform quadrant. The apoptosis of hippocampal neurons was detected by flow cytometry. By immunohistochemical staining and protein Immunohistochemistry was used to detect the expression of c-Jun protein in hippocampus of rats in each group. The expression of c-Jun protein was analyzed by bivariate analysis. Results Compared with NC group, learning and memory abilities decreased in COP group, DNS group and HBO group. Compared with NC group, learning and memory abilities of HBO group increased significantly (P <0.05). Compared with NC group, COP group, DNS group and HBO group The degree of neuronal apoptosis increased; the apoptosis of hippocampal neurons in HBO group decreased compared with that in DNS group. Compared with NC group, c-Jun protein expression in hippocampus of COP group, DNS group and HBO group increased (P <0.05); c-Jun protein expression in hippocampus of HBO group decreased compared with that in DNS group <0.05). Bivariate analysis showed that there was a positive correlation between c-Jun protein expression and mean escape latency in COP group, DNS group and HBO group, negatively correlated with the number of platform traversing and platform quadrant swimming distance. Conclusions Carbon monoxide exposure, especially delayed encephalopathy after carbon monoxide poisoning, can cause c-Jun protein overexpression, resulting in decreased learning and memory ability. Hyperbaric oxygen therapy can improve the learning and memory ability of rats with delayed encephalopathy after carbon monoxide poisoning, and its mechanism may be related to the regulation of c-Jun protein expression in hippocampus.