Hydrogen sulfide-releasing peptide attenuates autophagy-driven cellular injury in an experimental ischemic stroke model.

Ischemic stroke is often linked to increased oxidative stress, impaired autophagy, and resultant cellular injury. This study examines the correlation between autophagy-mediated cellular injury and the use of a hydrogen sulfide (H2S)-releasing peptide, SV-E4, to mitigate cellular damage resulting from oxygen-glucose deprivation (OGD), an in vitro model simulating ischemic stroke. The research employs neuroblastoma (N2a) and microglial (BV2) cell lines as well as 3-day developed chicken embryos. Elevated levels of pro-autophagic proteins corroborate our study's findings that OGD markedly enhances oxidative stress and triggers autophagy. Administration of the SV-E4 peptide formulation to cells subjected to OGD significantly reduced the amounts of reactive oxygen species. In the present investigation, dihydroethidium, Amplex Red, 2',7'-dichlorofluorescin diacetate, and mito-SOX were all utilized to corroborate conclusion. Decreased levels of autophagy markers indicated that the SV-E4 formulation could prevent aberrant autophagy. Notably, this mechanism is not limited to ischemic stroke but extends to other ischemia-reperfusion models, as demonstrated using an in ovo ischemia-reperfusion model in chicken embryos. Altogether, the results indicate that the SV-E4 peptide has a beneficial impact on preventing excessive oxidative stress and autophagy, demonstrating its potential as a treatment approach for individuals with ischemic stroke.