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目的:探讨氯胺酮对老龄大鼠认知功能、海马神经元凋亡以及海马组织p38蛋白表达的影响。方法:将42只健康老龄雄性Wistar大鼠随机分为A组(对照组)、B组(50 mg·kg-1氯胺酮)和C组(100 mg·kg-1氯胺酮),每组14只。腹腔注射生理盐水或氯胺酮后,采用Morris水迷宫实验评估大鼠的认知水平,原位末端标记(TUNEL)法观察海马神经元凋亡情况,Western blot检测海马组织p38蛋白表达水平。结果:Morris水迷宫测试显示,B组和C组逃避潜伏期都明显大于A组,且C组逃避潜伏期长于B组(P<0.05),C组在平台所在象限停留时间(21.17±6.93)s和跨过平台区域的次数(4.25±1.85)显著少于A组(32.97±4.86)s和(8.62±1.86)(P<0.05);B组(15.18±1.48)%和C组(20.52±5.86)%分别与A组(1.10±0.23)%比较,大鼠海马神经元凋亡率明显增加(P<0.05);氯胺酮麻醉后,大鼠海马组织p38蛋白表达显著增高,且C组明显高于B组(P<0.05)。结论:氯胺酮可致老龄大鼠认知功能损害,其机制可能与大鼠海马p38蛋白表达水平增高进而诱导海马神经元凋亡有关。
AIM: To investigate the effects of ketamine on cognitive function, apoptosis of hippocampal neurons and the expression of p38 in hippocampus of aged rats. Methods: Forty-two healthy male Wistar rats were randomly divided into A group (control group), B group (50 mg · kg -1 ketamine) and C group (100 mg · kg -1 ketamine), 14 in each group. After intraperitoneal injection of saline or ketamine, the level of cognition in hippocampal neurons was detected by Morris water maze test. The apoptosis of hippocampal neurons was observed by TUNEL method. The expression of p38 protein in hippocampus was detected by Western blot. Results: Morris water maze test showed that the evasive latency of group B and C were significantly greater than that of group A, and the evasive latency of group C was longer than that of group B (P <0.05). In group C, the mean residence time in the quadrant of platform was (21.17 ± 6.93) s and (4.25 ± 1.85) were significantly less than those in group A (32.97 ± 4.86) s and (8.62 ± 1.86) respectively (P <0.05); group B (15.18 ± 1.48)% and group C (20.52 ± 5.86) % Were significantly higher than those in group A (1.10 ± 0.23)%, respectively (P <0.05). After ketamine anesthesia, the expression of p38 protein in hippocampus of rats was significantly higher than that in group A Group (P <0.05). CONCLUSION: Ketamine can cause cognitive impairment in aged rats. The mechanism may be related to the increased expression of p38 protein in hippocampus and the apoptosis of hippocampal neurons.