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Protective effects of hydrogen sulfide in a rat model of traumatic brain injury via activation of mitochondrial adenosine triphosphate–sensitive potassium channels and reduction of oxidative stress

  • Author Footnotes
    1 Xiaofan Jiang and Yi Huang contributed equally to this work.
    Xiaofan Jiang
    Footnotes
    1 Xiaofan Jiang and Yi Huang contributed equally to this work.
    Affiliations
    Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi’an, Shaanxi Province, People’s Republic of China
    Search for articles by this author
  • Author Footnotes
    1 Xiaofan Jiang and Yi Huang contributed equally to this work.
    Yi Huang
    Footnotes
    1 Xiaofan Jiang and Yi Huang contributed equally to this work.
    Affiliations
    Department of Anesthesiology, Xiing Hospital, Fourth Military Medical University, Xi’an, Shaanxi Province, People’s Republic of China
    Search for articles by this author
  • Wei Lin
    Affiliations
    Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi’an, Shaanxi Province, People’s Republic of China
    Search for articles by this author
  • Dakuan Gao
    Affiliations
    Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi’an, Shaanxi Province, People’s Republic of China
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  • Zhou Fei
    Correspondence
    Corresponding author. Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi Province, P. R. China. Tel.: +86 29 84775323; fax: +86 29 84775567.
    Affiliations
    Department of Neurosurgery, Xijing Institute of Clinical Neuroscience, Xiing Hospital, Fourth Military Medical University, Xi’an, Shaanxi Province, People’s Republic of China
    Search for articles by this author
  • Author Footnotes
    1 Xiaofan Jiang and Yi Huang contributed equally to this work.
Published:April 10, 2013DOI:https://doi.org/10.1016/j.jss.2013.03.067

      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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