Ischemic preconditioning (IPC) induced by sublethal
transient cerebral ischemia could reduce neuronal damage/death following a subsequent lethal
transient cerebral ischemia. We, in this study, compared expressions of
interleukin (IL)-2 and
tumor necrosis factor (TNF)-α as pro-inflammatory
cytokines, and
IL-4 and
IL-13 as anti-inflammatory
cytokines in the gerbil hippocampal CA1 region between animals with lethal
ischemia and ones with IPC followed by lethal
ischemia. In the animals with lethal
ischemia, pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region were dead at 5 days post-
ischemia; however, IPC protected the CA1 pyramidal neurons from lethal ischemic injury. Expressions of all
cytokines were significantly decreased in the SP after lethal
ischemia and hardly detected in the SP at 5 days post-
ischemia because the CA1 pyramidal neurons were dead. IPC increased expressions of anti-inflammatory
cytokines (IL-4 and IL-13) in the stratum pyramidale of the CA1 region following no lethal
ischemia (
sham-operation), and the increased expressions of
IL-4 and
IL-13 by IPC were continuously maintained is the SP of the CA1 region after lethal
ischemia. However, pro-inflammatory
cytokines (IL-2 and TNF-α) in the SP of the CA1 region were similar those in the
sham-operated animals with IPC, and the
IL-4 and
IL-13 expressions in the SP were maintained after lethal
ischemia. In conclusion, this study shows that anti-inflammatory
cytokines significantly increased and longer maintained by IPC and this might be closely associated with neuroprotection after lethal
transient cerebral ischemia.