The present study has been designed to investigate the potential role of CCR-2
chemokine receptor in ischemic preconditioning as well as postconditioning induced reversal of
ischemia-reperfusion injury in mouse brain. Bilateral carotid artery occlusion of 17 min followed by reperfusion for 24h was employed in present study to produce
ischemia and reperfusion induced cerebral injury in mice.
Cerebral infarct size was measured using
triphenyltetrazolium chloride staining. Memory was evaluated using elevated plus-maze test and Morris water maze test. Rota rod test was employed to assess motor
incoordination. Bilateral carotid artery occlusion followed by reperfusion produced
cerebral infarction and impaired memory and motor co-ordination. Three preceding episodes of bilateral carotid artery occlusion for 1 min and reperfusion of 1 min were employed to elicit ischemic preconditioning of brain, while three episodes of bilateral carotid artery occlusion for 10s and reperfusion of 10s immediately after the completion of were employed to elicit
ischemic postconditioning of brain. Both prior ischemic preconditioning as well as
ischemic postconditioning immediately after global
cerebral ischemia prevented markedly
ischemia-reperfusion-induced cerebral injury as measured in terms of
infarct size, loss of memory and motor coordination.
RS 102895, a selective CCR-2
chemokine receptor antagonist, attenuated the
neuroprotective effect of both the ischemic preconditioning as well as postconditioning. It is concluded that the
neuroprotective effect of both ischemic preconditioning as well as
ischemic postconditioning may involve the activation of CCR-2
chemokine receptors.