Differential Expression of CXCL1, CXCL10, and CXCL12 in Response to Cerebral Ischemic Postconditioning in Rat Brain

Document Type : Original Articles


1 Physiology Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

2 Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.

3 Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.



Objectives: Cerebral ischemic preconditioning lessens stroke-induced injuries, but it is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role against cerebral injury after stroke; we tested the hypothesis that interrupting ischemia during early reperfusion, i.e. Postconditioning (POCO) affects CXC chemokine expression and further reduce inflammation in rat model of ischemia/reperfusion. Materials & Methods: Adult male Wistar rats (250-300 g) were used in this experiment. Using 4-vessel occlusion method, global cerebral ischemia was induced and POCO was performed by applying 3 cycles of 15-s/15-s reperfusion/reocclusion after a 45-s reperfusion (POCO-45-15/15). Western blotting analysis was used to investigate CXCL1, CXCL10 and CXCL12 expression 24 h, 48 h and one week after ischemic postconditioning (iPOCO).Results: Based on the results, iPOCO attenuates the expression of inflammatory chemokines CXCL1 and CXCL10 in hippocampus area of postconditioned rats, while the CXCL12 was not affected by iPOCO.Conclusion: Current findings may support chemokines role in iPOCO via reduction of inflammation. Also there could be a link between postconditioning, stress and inflammation through chemokines.


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