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对解偶联蛋白 2 缺陷小鼠进行麻醉和镇静分析表明，UCP2 在运动中起作用。

Analysis of uncoupling protein 2-deficient mice upon anaesthesia and sedation revealed a role for UCP2 in locomotion.

机构信息

INSERM U1016, CNRS UMR8104, Institut Cochin, Paris, France.

出版信息

PLoS One. 2012;7(8):e41846. doi: 10.1371/journal.pone.0041846. Epub 2012 Aug 10.

DOI:10.1371/journal.pone.0041846
PMID:22900002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3416814/
Abstract

General anaesthesia is associated with hypothermia, oxidative stress, and immune depression. Uncoupling Protein (UCP2) is a member of the mitochondrial carrier family present in many organs including the spleen, the lung and the brain. A role of UCP2 in the activation of the inflammatory/immune cells, in the secretion of hormones, and in the excitability of neurons by regulating the production of reactive oxygen species has been discussed. Because of the side effects of anaesthesia listed above, we aimed to question the expression and the function of UCP2 during anaesthesia. Induction of anaesthesia with ketamine (20 mg/kg) or isoflurane (3.6%) and induction of sedation with the α2 adrenergic receptor agonist medetomidine (0.2 mg/kg) stimulated infiltration of immune cells in the lung and increased UCP2 protein content in the lung, in both immune and non-immune cells. UCP2 content in the lung inversely correlated with body temperature decrease induced by medetomidine treatment. Challenge of the Ucp2(-/-) mice with isoflurane and medetomidine revealed an earlier behavioral recovery phenotype. Transponder analysis of body temperature and activity showed no difference between Ucp2(-/-) and control mice in basal conditions. However, upon an acute decrease of body temperature induced by medetomidine, Ucp2(-/-) mice exhibited increased locomotion activity. Together, these results show that UCP2 is rapidly mobilized during anaesthesia and sedation in immune cells, and suggest a role of UCP2 in locomotion.

摘要

全身麻醉与体温降低、氧化应激和免疫抑制有关。解偶联蛋白 2（UCP2）是一种位于许多器官中的线粒体载体家族的成员，包括脾脏、肺和大脑。已经讨论了 UCP2 在激活炎症/免疫细胞、激素分泌以及通过调节活性氧的产生来调节神经元兴奋性中的作用。由于上述麻醉的副作用，我们旨在质疑麻醉过程中 UCP2 的表达和功能。用氯胺酮（20mg/kg）或异氟烷（3.6%）诱导麻醉，用α2 肾上腺素能受体激动剂右美托咪定（0.2mg/kg）诱导镇静，刺激免疫细胞浸润肺部，并增加肺部的 UCP2 蛋白含量，在免疫和非免疫细胞中均如此。肺部的 UCP2 含量与右美托咪定治疗引起的体温下降呈负相关。用异氟烷和右美托咪定对 Ucp2(-/-)小鼠进行的挑战显示出更早的行为恢复表型。体温和活动的转发器分析显示，在基础条件下，Ucp2(-/-)和对照小鼠之间没有差异。然而，在用右美托咪定诱导急性体温下降时，Ucp2(-/-)小鼠表现出增加的运动活动。总之，这些结果表明 UCP2 在免疫细胞中快速动员在麻醉和镇静期间，并提示 UCP2 在运动中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/c24481a36f2e/pone.0041846.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/9d3182974ec0/pone.0041846.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/a84607c63755/pone.0041846.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/04bdc495d3a9/pone.0041846.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/e7409b8b63d4/pone.0041846.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/c24481a36f2e/pone.0041846.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/9d3182974ec0/pone.0041846.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/a84607c63755/pone.0041846.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/04bdc495d3a9/pone.0041846.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/e7409b8b63d4/pone.0041846.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa35/3416814/c24481a36f2e/pone.0041846.g005.jpg

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