Abstract
Background
Hydrogen sulfide (H2S) is considered an important neuromodulator in the central nervous system. We designed
the present study to investigate the effects of exogenous H2S in a rat model of traumatic brain injury (TBI) and the mechanism(s) that underlie
this effect.
Methods
We induced a TBI model by controlled cortical impact injury. We intraperitoneally
administered sodium hydrosulfide (NaHS) (an H2S donor) (3 mg/kg) or vehicle alone at 5 min after a TBI operation. We then measured
the H2S level, brain edema, blood-brain barrier integrity, neurologic dysfunction, and lesion
volume in all animals. Moreover, we assessed the role of mitochondrial adenosine triphosphate–sensitive
potassium (mitoKATP)channels by intraperitoneal injection of the selective blocker 5-hydroxydecanoate
before NaHS administration. In addition, we detected the levels of oxidative products
and the activities of antioxidant enzymes in brain tissue.
Results
Administration of NaHS significantly increased the H2S level of brain tissue in TBI-challenged rats. The TBI-challenged animals exhibited
significant brain injuries, characterized by an increase of blood-brain barrier permeability,
brain edema, and lesion volume, as well as neurologic dysfunction, which were significantly
ameliorated by NaHS treatment. However, the protective effects of H2S in TBI could be abolished by the mitoKATPchannel blocker 5-hydroxydecanoate. Moreover, we found that NaHS treatment increased
endogenous antioxidant enzymatic activities and decreased oxidative product levels
in brain tissue of TBI-challenged rats.
Conclusions
Exogenous H2S administered at an appropriate dose can exert a protective effect against TBI via
activation of mitoKATP channels and reduction of oxidative stress.
Keywords
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Article info
Publication history
Published online: April 10, 2013
Accepted:
March 20,
2013
Received in revised form:
March 19,
2013
Received:
January 6,
2013
Identification
Copyright
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.