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首页> 外文期刊>Cellular Physiology and Biochemistry >Repeated Administration of Ketamine can Induce Hippocampal Neurodegeneration and Long-Term Cognitive Impairment via the ROS/HIF-1α Pathway in Developing Rats
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Repeated Administration of Ketamine can Induce Hippocampal Neurodegeneration and Long-Term Cognitive Impairment via the ROS/HIF-1α Pathway in Developing Rats

机译：反复服用氯胺酮可通过发育中的大鼠通过ROS /HIF-1α途径诱导海马神经变性和长期认知障碍

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biBackground /i/bRecent animal experiments have suggested that ketamine administration during development might induce widespread neurodegeneration and long-term cognitive deficits. The underlying mechanism is not fully understood. biMethods /i/bImmature rat hippocampal neurons and newborn rats underwent repeated exposure to ketamine, ketamine+inhibitor of hypoxia-inducible factor (HIF)-1α(YC-1), ketamine+inhibitor of reactive oxygen species(ROS) (L-carnitine) or ketamine+Casup2+/sup blocker(nimodipine). Apoptosis of the hippocampal neurons was analyzed by TUNEL and flow cytometry. Intracellular ROS were measured using 2',7'-dichlorofluorescein diacetate. The expression of HIF- 1α and apoptosis-related proteins was analyzed by western blot or qPCR. As these rats grew, behavioral tests were performed to evaluate cognitive function. biResults /i/bThe apoptotic rate in the ketamine group was significantly higher than that in the other groups, and the intracellular ROS levels in the ketamine and ketamine+YC-1 groups were higher than those in the other groups. The expression of HIF- 1α, p53, BNIP3 and cleaved caspase-3 proteins increased, and the ratio of Bcl-2/Bax decreased in the ketamine group. The transcriptional levels of HIF-1α in the ketamine and ketamine+YC-1 groups were higher than those in the other groups. Cognitive deficits were found only in the ketamine group. biConclusion /i/bWe suggest that ketamine-induced neurodegeneration in neonatal rats, followed by long-term cognitive deficits, might be mediated via the ROS/HIF-1α pathway.
机译：背景 最近的动物实验表明，在发育过程中服用氯胺酮可能会引起广泛的神经变性和长期认知缺陷。潜在的机制尚不完全清楚。 方法 未成熟的大鼠海马神经元和新生大鼠反复暴露于氯胺酮，氯胺酮+缺氧诱导因子（HIF）-1α（YC-1）抑制剂，氯胺酮+抑制剂活性氧（ROS）（L-肉碱）或氯胺酮+ Ca 2 + 阻滞剂（尼莫地平）的含量。通过TUNEL和流式细胞仪分析海马神经元的凋亡。使用2'，7'-二氯荧光素二乙酸酯测量细胞内ROS。通过蛋白质印迹或qPCR分析HIF-1α和凋亡相关蛋白的表达。随着这些大鼠的成长，进行了行为测试以评估认知功能。 结果 氯胺酮组的细胞凋亡率显着高于其他组，氯胺酮和氯胺酮+ YC-1组的细胞内ROS水平高于其他组。其他组的人。氯胺酮组HIF-1α，p53，BNIP3和裂解的caspase-3蛋白的表达增加，而Bcl-2 / Bax的比率降低。氯胺酮和氯胺酮+ YC-1组中HIF-1α的转录水平高于其他组。仅在氯胺酮组中发现认知缺陷。 结论 我们建议，氯胺酮诱导的新生大鼠神经变性，继而引起长期的认知缺陷，可能是通过ROS /HIF-1α途径介导的。

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