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

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 & 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). 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. 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.