Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2–STAT3 pathway

Yanhua Chen,1,* Xu Zhang,2,* Bingdong Zhang,1 Guodong He,2 Lifang Zhou,2 Yubo Xie2 1Department of Anesthesiology, Cardiovascular Institute, 2Department of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China *These authors contributed equally to this work Abstr...

Full description

Saved in:
Bibliographic Details
Main Authors: Chen Y (Author), Zhang X (Author), Zhang B (Author), He G (Author), Zhou L (Author), Xie Y (Author)
Format: Book
Published: Dove Medical Press, 2017-09-01T00:00:00Z.
Subjects:
Online Access:Connect to this object online.
Tags: Add Tag
No Tags, Be the first to tag this record!

MARC

LEADER 00000 am a22000003u 4500
001 doaj_0c29f69319aa4db39d2a382f3d1a3e76
042 |a dc 
100 1 0 |a Chen Y  |e author 
700 1 0 |a Zhang X  |e author 
700 1 0 |a Zhang B  |e author 
700 1 0 |a He G  |e author 
700 1 0 |a Zhou L  |e author 
700 1 0 |a Xie Y  |e author 
245 0 0 |a Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2–STAT3 pathway 
260 |b Dove Medical Press,   |c 2017-09-01T00:00:00Z. 
500 |a 1177-8881 
520 |a Yanhua Chen,1,* Xu Zhang,2,* Bingdong Zhang,1 Guodong He,2 Lifang Zhou,2 Yubo Xie2 1Department of Anesthesiology, Cardiovascular Institute, 2Department of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China *These authors contributed equally to this work Abstract: Cardiopulmonary bypass (CPB) constitutes one of the primary methodologies pertaining to cardiac surgery. However, this form of surgery can cause damage to the body. Many studies have reported that dexmedetomidine confers cerebral protection. In this study, we aimed to investigate the effect and mechanism of dexmedetomidine on neuronal apoptosis caused by CPB. Here, rats were treated with different doses of dexmedetomidine by intravenous infusion 2 hours after CPB. We observed that dexmedetomidine treatment to rats reduces the S100ß, NSE levels in plasma, and neuronal apoptosis following CPB in a dose-dependent manner. Furthermore, we observed that the beneficial effect of dexmedetomidine treatment following CPB was associated with a reduction in IL6, an inflammatory cytokine in plasma and cortex. Our results suggest that dexmedetomidine provides neuroprotective effects by inhibiting inflammation and reducing neuronal apoptosis. There was a correlation between the protective effect on the brain and the dose of dexmedetomidine. In addition, dexmedetomidine administration inhibits phosphorylation of JAK2 and STAT3 proteins in the hippocampus of rats 2 hours after CPB. Therefore, we speculate that the JAK2–STAT3 pathway plays an important role in the neuroprotective effects of dexmedetomidine following brain injury induced by CPB. Keywords: apoptosis, cardiopulmonary bypass, dexmedetomidine, neuroprotective effect, JAK2, STAT3 
546 |a EN 
690 |a Apoptosis 
690 |a Cardiopulmonary bypass 
690 |a Dexmedetomidine 
690 |a Neuroprotective effect 
690 |a JAK2 
690 |a STAT3 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
655 7 |a article  |2 local 
786 0 |n Drug Design, Development and Therapy, Vol Volume 11, Pp 2787-2799 (2017) 
787 0 |n https://www.dovepress.com/dexmedetomidine-reduces-the-neuronal-apoptosis-related-to-cardiopulmon-peer-reviewed-article-DDDT 
787 0 |n https://doaj.org/toc/1177-8881 
856 4 1 |u https://doaj.org/article/0c29f69319aa4db39d2a382f3d1a3e76  |z Connect to this object online.