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Effects of different concentration and duration time of isoflurane on acute and long-term neurocognitive function of young adult C57BL/6 mouse.不同浓度和时长的异氟烷对年轻成年C57BL/6小鼠急性和长期神经认知功能的影响
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右美托咪定通过抗氧化、抗炎和抗凋亡作用减轻老龄大鼠异氟烷诱导的认知障碍。

Dexmedetomidine attenuates isoflurane-induced cognitive impairment through antioxidant, anti-inflammatory and anti-apoptosis in aging rat.

作者信息

Wang Xiaoning, Zhao Binjiang, Li Xue

机构信息

Department of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University Beijing, China.

Department of Anesthesiology, Peking University People's Hospital Beijing, China.

出版信息

Int J Clin Exp Med. 2015 Oct 15;8(10):17281-8. eCollection 2015.

PMID:26770320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4694220/
Abstract

As a kind of α2 adrenergic receptor agonists, dexmedetomidine generates sedation, anti-anxiety and anesthesia effects by hyperpolarizing noradrenergic nerve cells in locus coeruleus. This study was designed to investigate the neuroprotective of dexmedetomidine attenuates isoflurane-induced cognitive impairment, and the possible underlying mechanism in aging rat. Firstly, we used isoflurane-induced aging rat model to analyze the therapeutical effect of dexmedetomidine on cognitive impairment. Next, commercial ELISA kits were used to analyze tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), methane dicarboxylic aldehyde (MDA) and superoxide dismutase (SOD) and caspase-3 levels. In addition, Western blotting was used to detect the protein expression of P38 MAPK, PTEN and phosphorylation-Akt (p-Akt) expression. Our results showed that the neuroprotective of dexmedetomidine significantly attenuates isoflurane-induced cognitive impairment in aging rat. Moreover, dexmedetomidine significantly inhibited these TNF-α, IL-1β, MDA, SOD and caspase-3 activities in isoflurane-induced aging rat. Meanwhile, the neuroprotective effects of dexmedetomidine on isoflurane-induced cognitive impairment significantly suppressed Bcl-xL/Bad rate, P38 MAPK and PTEN protein expression and activated p-Akt protein expression in aging rat. Collectively, neuroprotective effect of dexmedetomidine attenuates isoflurane-induced cognitive impairment through antioxidant, anti-inflammatory and anti-apoptosis in aging rat.

摘要

作为一种α2肾上腺素能受体激动剂，右美托咪定通过使蓝斑中的去甲肾上腺素能神经细胞超极化产生镇静、抗焦虑和麻醉作用。本研究旨在探讨右美托咪定的神经保护作用是否能减轻异氟烷诱导的衰老大鼠认知障碍及其可能的潜在机制。首先，我们使用异氟烷诱导的衰老大鼠模型来分析右美托咪定对认知障碍的治疗效果。接下来，使用商业ELISA试剂盒分析肿瘤坏死因子α（TNF-α）、白细胞介素-1β（IL-1β）、丙二醛（MDA）、超氧化物歧化酶（SOD）和半胱天冬酶-3水平。此外，使用蛋白质印迹法检测P38丝裂原活化蛋白激酶（P38 MAPK）、磷酸酶和张力蛋白同源物（PTEN）以及磷酸化蛋白激酶B（p-Akt）的蛋白表达。我们的结果表明，右美托咪定的神经保护作用显著减轻了异氟烷诱导的衰老大鼠认知障碍。此外，右美托咪定显著抑制了异氟烷诱导的衰老大鼠中的这些TNF-α、IL-1β、MDA、SOD和半胱天冬酶-3活性。同时，右美托咪定对异氟烷诱导的认知障碍的神经保护作用显著抑制了衰老大鼠中的Bcl-xL/Bad比率、P38 MAPK和PTEN蛋白表达，并激活了p-Akt蛋白表达。总的来说，右美托咪定的神经保护作用通过抗氧化、抗炎和抗凋亡作用减轻了异氟烷诱导的衰老大鼠认知障碍。