• ISSN 1674-8301
  • CN 32-1810/R
Volume 27 Issue 4
Jul.  2013
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Article Contents
Hao Fan, Yu Guo, Xiaoyan Liang, Yibiao Yuan, Xiaohong Qi, Min Wang, Jianhua Ma, Hong Zhou. Hydrogen sulfide protects against amyloid beta-peptide induced neuronal injury via attenuating inflammatory responses in a rat model[J]. The Journal of Biomedical Research, 2013, 27(4): 296-304. doi: 10.7555/JBR.27.20120100
Citation: Hao Fan, Yu Guo, Xiaoyan Liang, Yibiao Yuan, Xiaohong Qi, Min Wang, Jianhua Ma, Hong Zhou. Hydrogen sulfide protects against amyloid beta-peptide induced neuronal injury via attenuating inflammatory responses in a rat model[J]. The Journal of Biomedical Research, 2013, 27(4): 296-304. doi: 10.7555/JBR.27.20120100

Hydrogen sulfide protects against amyloid beta-peptide induced neuronal injury via attenuating inflammatory responses in a rat model

doi: 10.7555/JBR.27.20120100
Funds:

This study was supported by the Priority Academic Program Development of Jiangsu Higher Education Institutions (No. Jx10131801095 to Hong Zhou).

  • Received: 2012-09-21
  • Issue Date: 2013-07-28
  • Neuroinflammation has been recognized to play a critical role in the pathogenesis of Alzheimer's disease (AD), which is pathologically characterized by the accumulation of senile plaques containing activated microglia and amyloid β-peptides (Aβ). In the present study, we examined the neuroprotective effects of hydrogen sulfide (H2S) on neuroinflammation in rats with Aβ1-40 hippocampal injection. We found that Aβ-induced rats exhibited a disorder of pyramidal cell layer arrangement, and a decrease of mean pyramidal cell number in the CA1 hippoc?ampal region compared with those in sham operated rats. NaHS (a donor of H2S, 5.6 mg/kg/d, i.p.) treatment for 3 weeks rescued neuronal cell death significantly. Moreover, we found that H2S dramatically suppressed the release of TNF-α, IL-1β and IL-6 in the hippocampus. Consistently, both immunohistochemistry and Western blotting assays showed that H2S inhibited the upregulation of COX-2 and the activation of NF-κB in the hippocampus. In conclusion, our data indicate that H2S suppresses neuroinflammation via inhibition of the NF-κB activation path?way in the Aβ-induced rat model and has potential value for AD therapy.

     

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