Isoflurane Postconditioning Upregulates Phosphorylated Connexin 43 in the Middle Cerebral Artery Occlusion Model and Is Probably Associated with the TGF-β1/Smad2/3 Signaling Pathway.

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-β1 (TGF-β1 (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-β1 (TGF-β1 (TGF-β1 (TGF-β1 (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 (P < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (P < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (P < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (β1 (TGF-P < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (β1 (TGF-P < 0.05). However, in the ISPOC group, damage of the brain was significantly ameliorated (β1 (TGF-β1 (TGF-P < 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-β1/Smad2/3 signaling pathway may be involved in the process.β1 (TGF.

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