L-Cysteine suppresses hypoxia-ischemia injury in neonatal mice by reducing glial activation, promoting autophagic flux and mediating synaptic modification via H2S formation

Publication date: Available online 8 May 2018 Source:Brain, Behavior, and Immunity Author(s): Danqing Xin, Xili Chu, Xuemei Bai, Weiwei Ma, Hongtao Yuan, Jie Qiu, Changxing Liu, Tong Li, Xin Zhou, Wenqiang Chen, Dexiang Liu, Zhen Wang We previously reported that L-Cysteine, an H2S donor, significantly alleviated brain injury after hypoxia-ischemic (HI) injury in neonatal mice. However, the mechanisms underlying this neuroprotective effect of L-Cysteine against HI insult remain unknown. In the present study, we tested the hypothesis that the protective effects of L-Cysteine are associated with glial responses and autophagy, and L-Cysteine attenuates synaptic injury as well as behavioral deficits resulting from HI. Consistent with our previous findings, we found that treatment with L-Cysteine after HI reduced early brain injury, improved behavioral deficits and synaptic damage, effects which were associated with an up-regulation of synaptophysin and postsynaptic density protein 95 expression in the lesioned cortex. L-Cysteine attenuated the accumulation of CD11b+/CD45high cells, activation of microglia and astrocytes and diminished HI-induced increases in reactive oxygen species and malondialdehyde within the lesioned cortex. In addition, L-Cysteine increased microtubule associated protein 1 light chain 3-II and Beclin1 expression, decreased p62 expression and phosphor-mammalian target of rapamycin and phosphor-signal transducer and activator of transcription 3. F...
Source: Brain, Behavior, and Immunity - Category: Neurology Source Type: research