Hydrogen sulfide offers neuroprotection on traumatic brain injury in parallel with reduced apoptosis and autophagy in mice

PLoS One. 2014 Jan 23;9(1):e87241. doi: 10.1371/journal.pone.0087241. eCollection 2014.

Abstract

Hydrogen sulfide (H2S), a novel gaseous mediator, has been recognized as an important neuromodulator and neuroprotective agent in the central nervous system. The present study was undertaken to study the effects of exogenous H2S on traumatic brain injury (TBI) and the underlying mechanisms. The effects of exogenous H2S on TBI were examined by using measurement of brain edema, behavior assessment, propidium iodide (PI) staining, and Western blotting, respectively. Compared to TBI groups, H2S pretreatment had reduced brain edema, improved motor performance and ameliorated performance in Morris water maze test after TBI. Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. The results suggest a protective effect and therapeutic potential of H2S in the treatment of brain injury and the protective effect against TBI may be associated with regulating apoptosis and autophagy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Apoptosis / drug effects*
  • Autophagy / drug effects*
  • Blotting, Western
  • Brain Edema / etiology
  • Brain Edema / pathology
  • Brain Injuries / drug therapy*
  • Hydrogen Sulfide / pharmacology*
  • Hydrogen Sulfide / therapeutic use
  • Maze Learning / drug effects
  • Mice
  • Motor Activity / drug effects
  • Neuroprotective Agents / pharmacology*
  • Neuroprotective Agents / therapeutic use
  • Propidium
  • Transcription Factor TFIIH
  • Transcription Factors / metabolism

Substances

  • Gtf2h1 protein, mouse
  • Neuroprotective Agents
  • Transcription Factors
  • Transcription Factor TFIIH
  • Propidium
  • Hydrogen Sulfide

Grants and funding

This study was supported by grants 30872666, 81172911 and 81301039 from the National Natural Science Foundation of China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.