Background: Although the neuroprotective effect of sodium hydrosulfide (NaHS, a hydrogen
sulfide donor) pretreatment has been revealed, the effect of NaHS post-conditioning remains
Objective: We aimed to investigate the neuroprotective effect of NaHS post-conditioning against
transient Global Cerebral Ischemia (tGCI)-induced hippocampal CA1 injury and its underlying
Methods: A tGCI rat model was established using the four-vessel occlusion method for 15 min of
ischemia. The survival of hippocampal neurons was determined by Nissl staining and NeuN immunostaining.
Protein expression of potassium voltage-gated channel subfamily D member 2 (Kv4.2)
and potassium channel interacting protein 3 (KChIP3) was assessed by Immunohistochemistry
(IHC) and Western blot.
Results: Decreased concentrations (12 and 24 µmol/kg) of NaHS post-conditioning significantly
increased the numbers of survival neurons and NeuN-positive neurons in the hippocampal CA1
region at 7 days post-tGCI (all P<0.05). NaHS post-conditioning (24 µmol/kg) at 12 and 24 hr posttGCI
can achieve the best protective effect (both P<0.05). IHC data demonstrated that NaHS postconditioning
(24 µmol/kg) markedly attenuated tGCI-induced down-regulation of Kv4.2 protein in
the hippocampal CA1 region at 26 hr post-tGCI. Confocal images showed that Kv4.2 did not express
in the neuronal nuclei but predominantly express in the neuronal dendrites. In addition, NaHS
post-conditioning significantly up-regulated Kv4.2 and down-regulated KChIP3 in tGCI rats at 26
and 168 hr post- tGCI (all P<0.05).
Conclusion: Decreased concentrations of NaHS post-conditioning at 12-24 hr post-tGCI effectively
protected hippocampal CA1 neurons from tGCI-induced injury, which may be through regulating
the expression of Kv4.2 and KChIP3.