Effect of exogenous hydrogen sulfide on neuronal apoptosis during focal cerebral ischemia-reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effect of exogenous hydrogen sulfide (H2S) on neuronal apoptosis during focal cerebral ischemia-reperfusion (I/R) in rats.Methods One hundred eight male Sprague-Dawley rats,aged 6-8 weeks,weighing 250-270 g,were randomly divided into 3 groups (n =36 each) using a random number table:control group (group C),I/R group and H2S group.Focal cerebral ischemia was induced by middle cerebral artery occlusion in anesthetized rats.A nylon thread with a rounded tip was inserted into the left internal carotid artery and advanced intracranially to block blood flow into the middle cerebral artery.Middle cerebral artery occlusion was maintained for 90 min followed by reperfusion.In group H2S,0.25％ NaSH (a donor of exogenous H2S) 10 mg/kg was injected intraperitoneally at the onset of reperfusion.The equal volume of normal saline was given in C and I/R groups.At 1,3 and 7 days of reperfusion,neurological deficit was scored,and corner test was performed.Brains were removed for determination of myocardial infarct size,Bax-,Bcl-2-and caspase-3-positive cells,and cell apoptosis.The percentage of myocardial infarct size,rate of Bax-,Bcl-2-and caspase-3-positive cells and apoptosis rate were calculated.Results Compared with group C,the neurological deficit score was significantly decreased,and the corner score,percentage of myocardial infarct size,rate of Bax-,Bcl-2-and caspase-3-positive cells and apoptosis rate were increased at each time point of reperfusion in I/R and H2S groups (P＜0.05).Compared with group I/R,the neurological deficit score and Bcl-2-positive cells were significantly increased,and the corner score,percentage of myocardial infarct size,rate of Bax-and caspase-3-positive cells and apoptosis rate were decreased at each time point of reperfusion in group H2S (P＜0.05).Conclusion The mechanism by which exogenous H2S attenuates focal cerebral I/R is related to inhibition of neuronal apoptosis in rats.