Research ReportIncreased phosphorylation of mTOR is involved in remote ischemic preconditioning of hippocampus in mice

- Renal ischemia preconditioning (RIPC) decreased neuronal apoptosis in hippocampus.
- RIPC improved memory defects after hippocampal ischemia.
- RIPC augmented p-mTOR expression after hippocampal ischemia.
- Rapamycin, mTOR inhibitor, abolished all above mentioned effects of RIPC.
- mTOR pathway is involved in RIPC induced protection.

Different signaling pathways are involved in tissue protection against ischemia reperfusion (IR) injury, among them mammalian target of rapamycin (mTOR) and related pathways have been examined in many recent studies. Present study evaluated the role of mTOR in remote ischemic preconditioning (RIPC) of hippocampus. Renal ischemia was induced (3 cycles of 5 min occlusion and 5 min reperfusion of unilateral renal artery) 24 h before global brain ischemia (20 min bilateral common carotid artery occlusion). Saline or rapamycin (mTOR inhibitor; 5 mg/kg, i.p.) was injected 30 min before RIPC. mTOR and phosphorylated mTOR (p-mTOR) expression, superoxide dismutase (SOD) activity and retention trial of passive avoidance test were determined 24 h after global ischemia. Apoptosis and neuronal cell density were assessed 72 h after hippocampal ischemia. RIPC decreased apoptosis (p<0.05 vs. IR), improved memory (p<0.05 vs. IR), and augmented p-mTOR expression and SOD activity after hippocampal ischemia (p<0.05 vs. IR). Rapamycin abolished all protective effects of RIPC (p<0.05 vs. RIPC+IR) suggesting a role for mTOR in RIPC induced hippocampal protection.

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