Remote ischemic perconditioning (RIPerC) and
ischemic postconditioning (IPOC) are well-acknowledged neuroprotective procedures during ischemic injury. The present study established a combined RIPerC and IPOC (RIPerC + IPOC) model in rats and studied how it would regulate the autophagy process and affect
HMGB1 levels in a rat model of
middle cerebral artery occlusion (MCAO). Rats with MCAO were treated with RIPerC by fastening and release of the left hind limb to achieve 4 cycles of 5 min remote
ischemia reperfusion, 40 min prior to cerebral reperfusion, and then treated with IPOC by exposing the cerebral middle artery to 3 cycles of 30 s reperfusion/30 s occlusion at the onset of cerebral reperfusion.
Infarction volumes, neurological deficits, and pathological changes were assessed 24 h after
ischemia. The autophagy activator
rapamycin (RAP) and the autophagy inhibitor
3-methyladenine (3-MA) were administrated for further mechanism. The expression and location of
HMGB1 and the
autophagy-related proteins like LC3,
Beclin1, and P62 as well as plasma
HMGB1 levels were measured. Our results suggested that RIPerC + IPOC attenuated plasma
HMGB1 levels to intensify its
neuroprotective effect against cerebral ischemic
reperfusion injury via inhibiting the autophagy process.