异氟醚后处理上调大脑中动脉闭塞模型中磷酸化连接蛋白 43 的表达，可能与 TGF-β1/Smad2/3 信号通路有关。
Isoflurane Postconditioning Upregulates Phosphorylated Connexin 43 in the Middle Cerebral Artery Occlusion Model and Is Probably Associated with the TGF-1/Smad2/3 Signaling Pathway.
机构信息
Department of Anesthesiology, First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi 832002, China.
Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
出版信息
Biomed Res Int. 2020 Mar 17;2020:3451215. doi: 10.1155/2020/3451215. eCollection 2020.
AIM
Connexin 43 (Cx43) has been identified to be important for cerebral ischemia/reperfusion (I/R) injury as well as protection from it. This study was aimed at investigating the relationship between phosphorylated Cx43 (p-Cx43), transforming growth factor-1 (TGF-1 (TGF.
METHODS
The middle cerebral artery occlusion (MCAO) model was induced in 96 male Sprague-Dawley rats, weighing 250-300 g. The rats were randomized into 12 groups, namely, sham, middle cerebral artery occlusion (MCAO)/I/R, I/R+1.5% ISPOC, I/R+LY2157299 (blocker of TGF-1 (TGF-1 (TGF-1 (TGF-1 (TGF.
RESULTS
Neurological deficit scores, brain infarct volume, and damaged neurons in the I/R group significantly increased compared to those in the sham group ( < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated ( < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated ( < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (1 (TGF- < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (1 (TGF- < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (1 (TGF-1 (TGF- < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (.
CONCLUSION
Isoflurane postconditioning (ISPOC) may alleviate cerebral I/R injury through upregulating the expression of p-Cx43, and the TGF-1/Smad2/3 signaling pathway may be involved in the process.1 (TGF.
目的
连接蛋白 43（Cx43）已被确定在脑缺血/再灌注（I/R）损伤以及对其的保护中起重要作用。本研究旨在探讨磷酸化 Cx43（p-Cx43）与转化生长因子-β1（TGF-β1）之间的关系。
方法
96 只雄性 Sprague-Dawley 大鼠（体重 250-300g）构建大脑中动脉闭塞（MCAO）模型。将大鼠随机分为 12 组，分别为假手术组、MCAO/I/R 组、I/R+1.5%ISPOC 组、I/R+LY2157299（TGF-β1 阻滞剂）组、I/R+ISPOC+LY2157299 组。
结果
与假手术组相比，I/R 组神经功能缺损评分、脑梗死体积和受损神经元明显增加（<0.05）。然而，ISPOC 组脑损伤明显改善（<0.05）。与 I/R 组相比，TGF-β1 抑制剂组的神经功能缺损评分、脑梗死体积和受损神经元明显增加（<0.05）。与 I/R 组相比，TGF-β1 抑制剂组的神经功能缺损评分、脑梗死体积和受损神经元明显增加（<0.05）。然而，ISPOC 组脑损伤明显改善（<0.05）。
结论
异氟醚后处理（ISPOC）可能通过上调 p-Cx43 的表达来减轻脑 I/R 损伤，TGF-β1/Smad2/3 信号通路可能参与了这一过程。
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