阿米洛利对氯胺酮麻醉大鼠神经细胞凋亡及神经细胞活性物质的影响

发布时间：2018-04-09 15:39

本文选题：阿米洛利　切入点：氯胺酮　出处：《中国老年学杂志》2017年13期

【摘要】：目的探讨阿米洛利对氯胺酮麻醉大鼠神经细胞凋亡及神经细胞活性物质的影响。方法选取60只成年雄性SD大鼠,根据随机数字表将大鼠分为生理盐水5 ml·kg~(-1)·h~(-1)组(对照组)、氯胺酮组40 mg·kg~(-1)·h~(-1),氯胺酮40 mg·kg~(-1)·h~(-1)+阿米洛利5.0 mg·kg~(-1)·h~(-1)组,每组20只,每天持续静脉注射2 h,连续给药7 d,最后1次给药24 h后应用Morris水迷宫测试各组大鼠空间记忆能力。水迷宫试验结束后处死各组大鼠取出脑海马组织,分别应用TUNEL法及免疫组化法检测神经元细胞凋亡指数及Bax、Bcl-2表达,酶联免疫吸附(ELISA)法测定海马组织匀浆中神经营养因子(NT)、神经生长因子(NGF)、脑源性神经营养因子(BDNF)及乙酰胆碱(Ach)水平。结果实验第1天氯胺酮组、氯胺酮+阿米洛利组逃避潜伏时间显著长于对照组(P0.05),随着实验时间延长,氯胺酮组、氯胺酮+阿米洛利组逃避潜伏期时间显著延长(P0.05),但氯胺酮+阿米洛利组各时间段逃避潜伏期时间均短于氯胺酮组(P0.05)。氯胺酮组、氯胺酮+阿米洛利组大鼠海马神经元细胞凋亡指数、Bax、Bcl-2阳性细胞数量均高于对照组(P0.05),而氯胺酮组大鼠海马神经元细胞凋亡指数、Bax、Bcl-2阳性细胞数量均高于氯胺酮+阿米洛利组(P0.05)。氯胺酮组海马匀浆中NT、NGF、BDNF、Ach水平低于氯胺酮+阿米洛利组(P0.05),而氯胺酮+阿米洛利组海马匀浆中NT、NGF、BDNF、Ach水平低于对照组(P0.05)。结论阿米洛利对氯胺酮麻醉后认知功能障碍的改善可能与其抑制神经细胞凋亡及调节神经细胞活性物质水平有关。
[Abstract]:Objective to investigate the effects of amiloride on neuronal apoptosis and neuronal activity in ketamine anesthetized rats.The spatial memory ability of rats in each group was measured by Morris water maze after 24 hours of continuous intravenous injection for 7 days.After the water maze test, the rats in each group were killed to take out the brain tissue, and the apoptotic index of neurons and the expression of Baxon Bcl-2 were detected by TUNEL method and immunohistochemical method, respectively.The levels of neurotrophic factors (NTN), nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and acetylcholine (ache) in hippocampal homogenate were determined by enzyme linked immunosorbent assay (Elisa).Results on the first day of the experiment, the escape latency of ketamine group and amiolol group was significantly longer than that of control group (P 0.05).The escape latency time of ketamine amilolol group was significantly longer than that of ketamine amilolol group, but the escape latency time of ketamine amilolol group was shorter than that of ketamine group.Ketamine group,The number of apoptotic cells of hippocampal neurons in ketamine amilolol group was higher than that in control group (P 0.05), while that in ketamine group was higher than that in ketamine group (P 0.05).The level of BDNFAch in the hippocampus homogenate of ketamine group was lower than that in ketamine amilolil group (P 0.05), while the level of NTNGF BDNFN Ach in ketamine amilolil group was lower than that in control group (P 0.05).Conclusion the improvement of cognitive dysfunction after ketamine anesthesia may be related to the inhibition of neuronal apoptosis and regulation of nerve cell active substances.
【作者单位】：南阳市中心医院麻醉科;
【基金】：河南省科技厅科技发展计划(No.14A320003)
【分类号】：R614

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