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Sevoflurane Postconditioning Reduces Apoptosis by Activating the JAK-STAT Pathway After Transient Global Cerebral Ischemia in Rats

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Author(s)
Kim, Hyun-ChangKim, EugeneBae, Jung IlLee, Kook HyunJeon, Young-TaeHwang, Jung-WonLim, Young-JinMin, Seong-WonPark, Hee-Pyoung
Keimyung Author(s)
Kim, Hyun Chang
Department
Dept. of Anesthesiology & Pain Medicine (마취통증의학)
Journal Title
Journal of Neurosurgical Anesthesiology
Issued Date
2017
Volume
29
Issue
1
Abstract
Background: The antiapoptotic effects of sevoflurane postconditioning are responsible for neuroprotection against cerebral ischemia-reperfusion injury. Phosphorylation of the Janus family tyrosine kinases (JAK) 2-signal transducers and activators of transcription (STAT) 3 pathway is linked to antiapoptosis. Here, we determined whether the antiapoptotic effects of sevoflurane postconditioning are associated with activation of the JAK2-STAT3 pathway after global transient cerebral ischemia in rats.

Materials and Methods: Forty-five rats were randomly assigned to 5 groups: sham (n=5), control (10 min of ischemia, n=10), sevoflurane postconditioning (2 periods of sevoflurane inhalation after ischemia for 10 min, n=10), AG490 (a JAK2 selective inhibitor, intraperitoneal administration of 40 mg/kg before ischemia, n=10), and sevoflurane postconditioning plus AG490 group (n=10). The number of apoptotic cells as well as the expression of JAK2, phosphorylated JAK2 (P-JAK2), STAT3, phosphorylated STAT3 (P-STAT3), Bcl-2 (antiapoptotic protein), and Bax (proapoptotic protein) were evaluated 3 days after ischemia.

Results: The apoptotic cell count was significantly lower in the sevoflurane postconditioning group than in the control, AG490, and sevoflurane postconditioning plus AG490 groups. JAK2 and STAT3 levels were comparable among all 5 groups. P-JAK2, P-STAT3, and Bcl-2 levels were higher and Bax levels were lower in the sevoflurane postconditioning group relative to the control, AG490, and sevoflurane postconditioning plus AG490 groups.

Conclusions: Sevoflurane postconditioning reduced apoptosis by increasing P-JAK and P-STAT expression after transient global ischemia in rats, and AG490 reversed the beneficial antiapoptotic effects of sevoflurane postconditioning, suggesting that the JAK-STAT pathway may be involved in the antiapoptotic mechanism of sevoflurane postconditioning.
Keimyung Author(s)(Kor)
김현창
Publisher
School of Medicine
Citation
Kim, Hyun-Chang et al. (2017). Sevoflurane Postconditioning Reduces Apoptosis by Activating the JAK-STAT Pathway After Transient Global Cerebral Ischemia in Rats. Journal of Neurosurgical Anesthesiology, 29(1), 37–45. doi: 10.1097/ANA.0000000000000331
Type
Article
ISSN
0898-4921
Source
https://insights.ovid.com/pubmed?pmid=27337676
DOI
10.1097/ANA.0000000000000331
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/32801
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Anesthesiology & Pain Medicine (마취통증의학)
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