Intracerebral hemorrhage (ICH) has extremely high morbidity and mortality, substantially impacting public health. Studying the pathophysiological mechanisms of ICH is a complicated undertaking, and there remains a lack of effective medical treatment for improving ICH survival rates and promoting recovery. This review describes the preclinical studies of intracerebral hemorrhage that have been performed to date in detail, including different methods used to establish animal models and identify the cellular mechanisms involved after ICH. Recently, it was reported that the endogenous hydrogen sulfide (H2S) pathway is downregulated in the brain after ICH. Thus, exogenous H2S may have therapeutic potential by rescuing the decreased levels of endogenous H2S level after injury. Furthermore, we also discuss the molecular mechanisms involved in the protective effects of H2S and how these effects may have therapeutic use to treat and prevent ICH-induced neuronal injury.
Keywords: Cell death; Ferroptosis; Hydrogen sulfide; Intracerebral hemorrhage; Pyroptosis.