Therapeutic effects of L-Cysteine in newborn mice subjected to hypoxia-ischemia brain injury via the CBS/H₂S system: Role of oxidative stress and endoplasmic reticulum stress.

ABSTRACT: Neonatal hypoxic-ischemic (HI) injury is a major cause of neonatal death and neurological dysfunction. H₂S has been shown to protect against hypoxia-induced injury and apoptosis of neurons. L-Cysteine is catalyzed by cystathionine-β-synthase (CBS) in the brain and sequentially produces endogenous H₂S. The present study was designed to investigate whether L-Cysteine could attenuate the acute brain injury and improve neurobehavioral outcomes following HI brain injury in neonatal mice by releasing endogenous H₂S. L-Cysteine treatment significantly attenuated brain edema and decreased infarct volume and neuronal cell death, as shown by a decrease in the Bax/Bcl-2 ratio, suppression of caspase-3 activation, and reduced phosphorylation of Akt and ERK at 72h after

SUBMITTER: Liu S 

PROVIDER: S-EPMC5524226 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature