Hydrogen sulfide (H(2)S), a well-known toxic gas, is regarded as endogenous
neuromodulator and plays multiple roles in the central nervous system under physiological and pathological states, especially in secondary neuronal injury. Recent studies have shown relatively high concentrations of
hydrogen sulfide (H(2)S) in the brain and also cytoprotective effects of endogenous and exogenous H(2)S in models of in vitro and in vivo ischemic injury. H(2)S protects neurons by functioning as an
anti-oxidant, anti-inflammatory, and anti-apoptotic mediator and by improving neurological function. Moreover, it protects neurons from
glutamate toxicity. Therefore, the present study aimed to determine whether H(2)S provides protection in transient focal
cerebral ischemia. Focal
ischemia was induced by 60-min
middle cerebral artery occlusion (MCAO), followed by 23-h reperfusion. Saline as a vehicle and
NaHS (H(2)S donor; 1 and 5 mg) were intraperitoneally injected (IP) at the beginning of
ischemia.
Infarct volume,
brain edema, and apoptosis were assessed 24 h after MCAO.Treatment with
NaHS at doses of 1 and 5 mg markedly reduced total
infarct volumes by 29 and 51 %, respectively (P < 0.001). In addition,
NaHS at doses of 1 and 5 mg reduced
brain edema (P < 0.05) and inhibited apoptosis by decreasing positive TUNEL cells (P < 0.001).The present study shows that treatment with H(2)S reduces
brain injuries and postischemic
cerebral edema in a dose-dependent manner likely through the blocking programmed cell death.We propose that H(2)S might be a promising therapeutic target for
stroke, although more researches are necessary to take into account the potential
therapeutic effects of H(2)S in
stroke patients.