Hydrogen sulfide improved learning and memory deficits by reversing the inhibition of methylmercuric chloride on BDNF/TrkB signaling pathway.

Objective: Methylmercuric chloride (MMC) has neurotoxicity, while hydrogen sulfide (H2S) has shown inhibitory properties against nerve damage induced by various factors. The study aimed to investigate the impact of H2S on MMC-induced learning and memory impairment in mice and to explore the underlying mechanisms.

Methods: A mouse model of learning and memory impairment was established by MMC gavage, and sodium hydrosulfide (NaHS) was used as an H2S donor for intervention.

The effect of hypoxia on Hydrogen Sulfide concentration of brain tissue in AD transgenic mice and its mechanism.

Objective: Research has shown that hydrogen sulfide (H2S) plays a protective role in many diseases of the nervous system. The aim of this study is to investigate the effect of hypoxia on endogenous H2S concentration in the cerebral cortex of Alzheimer's disease (AD) transgenic mice and its mechanism.

Methods: AD transgenic mice were raised in closed boxes and pure nitrogen was introduced to reduce the oxygen concentration to 8%-10%, establishing an animal model of hypoxia.

Calcium sensing receptor mediated the excessive generation of β-amyloid peptide induced by hypoxia in vivo and in vitro.

Hypoxia played an important role in the pathogenesis of AD. Hypoxia increased Aβ formation, then caused Alzheimer's disease. Calcium sensing receptor (CaSR) was involved in the regulation of cell growth, differentiation, hormonal secretion and other physiological function.

Hydrogen sulfide prevents OGD/R-induced apoptosis via improving mitochondrial dysfunction and suppressing an ROS-mediated caspase-3 pathway in cortical neurons.

Hydrogen sulfide (H2S), an endogenous gaseous mediator, has been shown to have protective effects against neuronal damage caused by brain ischemia. In this study, we explored the potential effects of H2S on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal apoptosis and the possible mechanisms. We find that sodium hydrosulfide (NaHS, a donator of H2S) prevents OGD/R-induced intracellular reactive oxygen species (ROS) elevation and activation of caspase-3 in cultured mouse cortical neurons.