[P-JAK2 and P-STAT3 protein expression and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats]

Nan Fang Yi Ke Da Xue Xue Bao. 2007 Feb;27(2):208-11, 218.
[Article in Chinese]

Abstract

Objective: To investigate the changes in phosphorylated JAK2 and STAT3 protein expression of and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats.

Methods: A rat models of focal cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion using modified filament method. Immunohistochemistry and Western blot analysis were used to detect the expression of P-JAK2 and P-STAT3 proteins, and TUNEL assay was employed to examine the cell apoptosis.

Results: P-JAK2 and P-STAT3 protein expression increased significantly after cerebral ischemia-reperfusion injury in rats. The immunoreactivity was prominent in the peripheral of the ischemic region and reached the peak level at 24 h of reperfusion, followed by slight decrement. The apoptotic cells increased obviously after cerebral ischemia-reperfusion injury, also reaching the peak level at 24 h of reperfusion.

Conclusion: The expression of phosphorylated JAK2 and STAT3 may be involved in the ischemic cellular events including apoptosis. JAK2/STAT3 signaling pathway plays a role in the pathophysiological process of cerebral ischemia/reperfusion cell injury and repair.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Apoptosis*
  • Blotting, Western
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Infarction, Middle Cerebral Artery / physiopathology*
  • Janus Kinase 2 / metabolism*
  • Male
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / genetics
  • Reperfusion Injury / physiopathology*
  • STAT3 Transcription Factor / metabolism*

Substances

  • STAT3 Transcription Factor
  • Janus Kinase 2