[P-JAK2 and P-STAT3 protein expression and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats].
Huifang Xie, Ruxiang Xu, Ji-peng Wei, Xiao-dan Jiang, Zhenhua Liu
Abstract
Huifang Xie, Ruxiang Xu, Ji-peng Wei, Xiao-dan Jiang, Zhenhua Liu
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.
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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.
Key concepts: Ischemia, Reperfusion injury, TUNEL assay, Apoptosis, Medicine, Western blot, STAT3, Immunohistochemistry