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To investigate the interaction and involvement of sodium hydrosulfide (NaHS),a H2S donor,on hippocampus of rats suffering from sepsis-associated encephalopathy,rats were subjected to cecal ligation and puncture (CLP)-induced sepsis.Adult male Sprague-Dawley rats were randomly divided into four groups:Sham group,CLP group,CLP+NaHS group and CLP+aminooxyacetic acid (AOAA,an inhibitor of H2S formation) group.The four groups were observed at 3,6,9,12 h after treatment.We examined hippocampal H2S synthesis and the expression of cystathionine-β-synthetase (CBS),a major enzyme involved in the H2S synthesis in hippocampus.CBS expression was detected by reverse transcription polymerase chain reaction (RT-PCR).The concentrations of inflammatory cytokines (TNF-α,IL-1β) were determined in hippocampus by using enzyme-linked immunosorbent assay (ELISA).Neuronal damage was studied by histological examination of hippocampus.In CLP group,H2S synthesis was significantly increased in hippocampus compared with sham group and it peaked 3 h after CLP (P＜0.05).Sepsis also resulted in a significantly upregulated CBS mRNA in hippocampus.The levels of TNF-α and IL-1β in the hippocampus were substantially elevated at each time point of measurement (P＜0.05),and they also reached a peak value at about 3 h.Administration of NaHS significantly aggravated sepsis-associated hippocampus inflammation,as evidenced by TNF-α and IL-1β activity and histological changes in hippocampus.In septic rats pretreated with AOAA,sepsis-associated hippocampus inflammation was reduced.It is concluded that the rats subjected to sepsis may suffer from brain injury and elevated pro-inflammatory cytokines are responsible for the process.Furthermore,administration of H2S can increase injurious effects and treatment with AOAA can protect the brain from injury.