Aim: To observe the neuroprotective effect of limb ischemic post-conditioning (LIPC) on local brain ischemia and reperfusion injury in rat, and to investigate whether mitochondrial ATP sensitive potassium channel (mito K(ATP)) and kappa-opioid receptor were involved in the neuroprotection.
Methods: Rats were randomly divided into 6 groups that were ischemia/reperfusion group, unilateral hindlimb ischemia group (uLIPC), bilateral hindlimbs ischemia group (bLIPC), bLIPC + antagonist of kappa-opioid receptor nor-binaltorphimine (nor-BNI) group, bLIPC + mito K(ATP) blocker 5-hydroxydecanoate(5-HD) group, bLIPC + extracorporeal circulation of bilateral hindlimbs via femoral arteries (EC) group. Cerebral ischemia was induced by middle cerebral artery occlusion (MCAO), neurological scores, plasma levels of dynorphin and enkephalin, the brain infarct areas were determined after reperfusion.
Results: Unilateral LIPC partially improved the neurological score after local brain ischemia and reperfusion injury in rat (P < 0.05), and decreased the infarct area compared with the untreated group undergoing brain ischemia and reperfusion (P < 0.01). Bilateral LIPC significantly improved the neurological score after local brain ischemia and reperfusion injury (P < 0.01), and decreased the infarct area (P < 0.01). The neurological scores of bilateral LIPC group were significant higher than those of unilateral LIPC (P < 0.05). The plasma level of dynorphin was significantly increased (P < 0.01) at 5, 15, 30 min, 1 and 2 h after bilateral LIPC, however, it deceased to the normal level at 12 h after bilateral LIPC. The plasma level of enkephalin showed no obvious change after bilateral LIPC (P > 0.05). nor-BNI (25 nmol/L) and 5-HD (10 mg/kg) abolished the effect of bilateral LIPC (P < 0.01).
Conclusion: LIPC protects rat from local brain ischemia and reperfusion injury. Mito K(ATP) may be involved in the neuroprotection, and kappa-opioid receptor may also participate in the protective effect.