首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >POSTTRAUMATIC ADMINISTRATION OF A SUB-ANESTHETIC DOSE OF KETAMINE EXERTS NEUROPROTECTION VIA ATTENUATING INFLAMMATION AND AUTOPHAGY
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POSTTRAUMATIC ADMINISTRATION OF A SUB-ANESTHETIC DOSE OF KETAMINE EXERTS NEUROPROTECTION VIA ATTENUATING INFLAMMATION AND AUTOPHAGY

机译:通过衰减炎症和自噬施用亚麻醉剂量的氯胺酮的次麻醉剂量

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As a complex disease, traumatic brain injury (TBI) can result in long-term psychiatric changes and sensorimotor and cognitive impairments. The TBI-induced loss of memory and long-term cognitive dysfunction are related to mechanistic factors including an increased inflammatory response, autophagy, edema, and ischemia. Many published studies have offered evidence for the neuroprotective effects and anti-inflammatory properties of ketamine for TBI patients. Nonetheless, there is a limited understanding of the accurate mechanism that underlies the potential neuroprotective effects of ketamine. Herein, it can be shown that posttraumatic administration of ketamine at a sub anesthetic dose (10 mg/kg ketamine, every 24 h up to 7 days) can prevent the TBI-induced production of IL-6 and TNF-alpha, attenuate deficits of dendrites and spines and exert beneficial effects on memory and behavior. Moreover, studies show that ketamine may activate the mTOR signaling pathway by p-mTOR induction to down-regulate the expression of crucial autophagic proteins such as LC3 and Beclin-1. According to these findings, ameliorating secondary brain injury and anti-inflammatory properties is closely related to the neuroprotection of ketamine, which supports the use of ketamine as a potential therapy for patients with TBI to alleviate functional deficits. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
机译:作为一种复杂的疾病,创伤性脑损伤(TBI)可导致长期的精神病变化和传感器和认知障碍。 TBI诱导的记忆丧失和长期认知功能障碍与机械因子有关,包括增加的炎症反应,自噬,水肿和缺血。许多公开的研究提供了TBI患者的神经保护作用和抗炎症性能的证据。尽管如此,对氯胺酮潜在神经保护作用的准确机制有限地了解。这里,可以证明,在副麻醉剂量(10mg / kg氯胺酮中,每24小时每24小时,每24小时,每24小时最高7天)的预先施用氯胺酮可以预防IL-6和TNF-α的产生,衰减缺陷树突和刺,对记忆力和行为产生有益影响。此外,研究表明,氯胺酮可以通过P-MTOR诱导激活MTOR信号传导途径,降低诸如LC3和BECLIN-1的关键自噬蛋白的表达。根据这些发现,改善的继发性脑损伤和抗炎性质与氯胺酮的神经保护密切相关,这支持氯胺酮作为TBI患者减轻功能性缺陷的潜在治疗。 (c)2016年IBRO。 elsevier有限公司出版。保留所有权利。

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