Effects of Exogenous Hydrogen Sulfide on Apoptosis Proteins and Oxidative Stress in the Hippocampus of Rats Undergoing Heroin Withdrawal

In this study, the mechanism of H2S protection in the hippocampus of heroin-treated rats was investigated. Male Sprague-Dawley rats were randomly divided into three groups: a saline group, a heroin and saline group, and a heroin and sodium hydrosulfide group. According to the principle of increasing heroin dosage daily, heroin withdrawal was precipitated on day 9 with an injection of naloxone (5 mg/kg, i.p.), and withdrawal symptoms were scored. The levels of cystathionine-beta-synthase, H2S, reduced glutathione and malondialdehyde, as well as the levels of cleaved caspase-3, Bax, and Bcl-2 proteins and the activities of superoxide dismutase, catalase, and glutathione peroxidase were assayed in the hippocampus. The results showed that exogenous H2S alleviated heroin withdrawal symptoms. Moreover, exogenous H2S not only increased cellular H2S and the cystathionine-beta-synthase protein level activity but also significantly improved heroin-induced oxidative stress. Protein expression of cleaved caspase-3 and Bax decreased, whereas Bcl-2 protein levels in hippocampus increased with exogenous H2S. Exogenous H2S alleviated heroin-induced rat hippocampal damage through antioxidant and antiapoptosis effects.