• J Neurosurg Anesthesiol · Jan 2017

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

    • Hyun-Chang Kim, Eugene Kim, Jung Il Bae, Kook Hyun Lee, Young-Tae Jeon, Jung-Won Hwang, Young-Jin Lim, Seong-Won Min, and Hee-Pyoung Park.
    • *Department of Anesthesiology and Pain Medicine, Keimyung University Dongsan Hospital, Keimyung University College of Medicine †Department of Anesthesiology and Pain Medicine, Hospital of Catholic University of Daegu, Daegu ‡Department of Anesthesiology and Pain Medicine, Seoul National University Hospital ∥Department of Anesthesiology and Pain Medicine, SMG-SNU Boramae Medical Center, Seoul National University College of Medicine, Seoul §Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea.
    • J Neurosurg Anesthesiol. 2017 Jan 1; 29 (1): 37-45.

    BackgroundThe 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 MethodsForty-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.ResultsThe 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.ConclusionsSevoflurane 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.

      Pubmed     Full text   Copy Citation     Plaintext  

      Add institutional full text...

    Notes

     
    Knowledge, pearl, summary or comment to share?
    300 characters remaining
    help        
    You can also include formatting, links, images and footnotes in your notes
    • Simple formatting can be added to notes, such as *italics*, _underline_ or **bold**.
    • Superscript can be denoted by <sup>text</sup> and subscript <sub>text</sub>.
    • Numbered or bulleted lists can be created using either numbered lines 1. 2. 3., hyphens - or asterisks *.
    • Links can be included with: [my link to pubmed](http://pubmed.com)
    • Images can be included with: ![alt text](https://bestmedicaljournal.com/study_graph.jpg "Image Title Text")
    • For footnotes use [^1](This is a footnote.) inline.
    • Or use an inline reference [^1] to refer to a longer footnote elseweher in the document [^1]: This is a long footnote..

    hide…

What will the 'Medical Journal of You' look like?

Start your free 21 day trial now.

We guarantee your privacy. Your email address will not be shared.