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Published:
Mar 4, 2016DOI:
10.4314/tjpr.v15i2.7Keywords:
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Main Article Content
A Study on Expression and Tyrosine 705 phosphorylation of STAT3 in Focal Cerebral Ischemia-Reperfusion Rat Model and its Role in Neuronal Apoptosis
Abstract
Purpose: To investigate the expression and tyrosine 705 phosphorylation of STAT3 in focal cerebral ischemia-reperfusion rat model and its role in neuronal apoptosis.
Methods: Ischemia-reperfusion model was established by thread-occluded method. Tetrazolium red (TTC), H/E and Nissl staining were used to evaluate whether ischemia-reperfusion model was successfully established. TUNEL staining and immunohistochemistry were employed to monitor apoptosis-positive nerve cells as well as STAT3-, p-Tyr705-STAT3-, Bcl-2- and Fas-positive cells in ischemic penumbra (IP) and ischemic core (IC).
Results: The results of TTC, HE and Nissl staining indicated that the ischemia reperfusion model was successfully established. After 3 h, ischemia followed by different reperfusion times, the STAT3-, p- Tyr705-STAT3-, Fas- and Bcl-2 positive cells counts and the apoptosis-positive nerve cells count were significantly (p < 0.05 or 0.01) increased to 27.20, 29.20, 15.90, 18.50, and 202.00 in IP and 19.50, 21.20, 12.50, 12.40, and 97.80 in IC, compared with the sham-operated group. As reperfusion times increased, cell counts did not decrease significantly relative to control group. Correlation analysis indicate that there was significant (p < 0.01) positive correlations among STAT3-, p-Tyr705 STAT3-, Fas- and Bcl-2-positive cells counts on the one hand, and apoptosis positive nerve cells count in IP and IC, on the other hand.
Conclusion: Regulating expression and tyrosine 705 phosphorylation of STAT3 may be a new and effective strategy for treating cerebral infarction.
Keywords: Ischemia-reperfusion, Neuronal apoptosis, STAT3, Phosphorylation, Cerebral infarction
