The role of nitric oxide on ischemic hippocampus during renal ischemic preconditioning

Remote ischemic preconditioning (RIPC) is an episode of intermittent sub lethal and brief ischemia in one organ, which causes protection against severe ischemia in another remote organ. The main purpose of this study was to assess the relevance of nitric oxide (NO) in renal ischemic preconditioning during brain ischemia-reperfusion in hippocampal tissue.

60 male BALB/C mice weighting 30-35g randomly were divided into six groups. Sham-operated group, IPC group (transient renal ischemia), IR group (global brain ischemia), RIPC (IPC+IR) group, L-NAME + IPC + IR group (L-NAME was injected 30 min before RIPC), L-NAME + sham + IR group. Three days after brain ischemia, the cell density in hippocampal CA1 subregion and the level of nitric oxide (NO) in hippocampus tissue were measured in different groups.

RIPC prevented the reduction in cell density in hippocampal CA1 area following ischemia (p ≤ 0.05). The level of nitric oxide was significantly increased in the hippocampus in comparison with the IR group (p ≤ 0.05). L-NAME reversed the protective effects of RIPC on ischemic hippocampal damage by inhibition of nitric oxide (p ≤ 0.01).

Increased nitric oxide during RIPC can protect the hippocampus against damage caused by ischemia-reperfusion.