Hydrogen sulfide protects focal cerebral ischemia-reperfusion injury in rats through the PI3K/Akt signaling pathway

A rat model of left middle cerebral artery occlusion was established. Rats were randomly divided into four groups: sham operation, ischemia-reperfusion (I/R), NaHS+I/R and inhibitor groups. HE staining showed that the neuronal structures were normal in the sham group. The extracellular space broadened and the number of neurons significantly reduced in the I/R group. Neuronal injury improved and the number of neurons increased after NaHS administration. Neuronal injury showed no significant change and the number of neurons decreased after the application of the Akt inhibitor wortmannin. The apoptotic rate of hippocampal neurons was detected using the TUNEL fluorescence staining assay. Results showed that the number of apoptotic cells significantly increased in the I/R group, but this number decreased after the application of NaHS. The number of apoptotic cells increased in the inhibitor group. The protective effect of NaHS was blocked by I/R. The change in pAkt expression was not obvious after I/R. The expression levels of caspase-9 and caspase-3 increased. NaHS increased the expression of I/R injury neurons but decreased the expression of caspase-9 and caspase-3. The protein expression of pAkt decreased in the inhibitor group. The expression levels of caspase-9 and caspase-3 increased. These results suggest that hydrogen sulfide can inhibit apoptosis and protect focal cerebral ischemia-reperfusion injury by activating phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.