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  • ISSN 1674-8301
  • CN 32-1810/R
Volume 27 Issue 5
Aug.  2013
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Jun Wang, Wenyi Qian, Qing Zhu, Jian Chen, Fei Huan, Rong Gao, Hang Xiao. Martentoxin, a large-conductance Ca2+-activated K+ channel inhibitor, attenuated TNF-α-induced nitric oxide release by human umbilical vein endothelial cells[J]. The Journal of Biomedical Research, 2013, 27(5): 386-393. DOI: 10.7555/JBR.27.20120080
Citation: Jun Wang, Wenyi Qian, Qing Zhu, Jian Chen, Fei Huan, Rong Gao, Hang Xiao. Martentoxin, a large-conductance Ca2+-activated K+ channel inhibitor, attenuated TNF-α-induced nitric oxide release by human umbilical vein endothelial cells[J]. The Journal of Biomedical Research, 2013, 27(5): 386-393. DOI: 10.7555/JBR.27.20120080
shu

Martentoxin, a large-conductance Ca2+-activated K+ channel inhibitor, attenuated TNF-α-induced nitric oxide release by human umbilical vein endothelial cells

  • Department of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 210029, China.

Funds: 

This work was supported by the National Science Foundation of China (No. 30271137

No. 30771831

No. 81072329) and the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)

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  • Received Date: July 22, 2012
    Graphical Abstract
    • Abstract
  • Martentoxin, a 4,046 Da polypeptide toxin purified from the venom of the scorpion Buthus martensii Karsch, has been demonstrated to block large-conductance Ca2+-activated K+ (BKCa) channels; however, its biological roles are still largely unknown. In the present study, we investigated the pharmacological effects of martentoxin on regulating the production of nitric oxide induced by TNF-α in human umbilical vein endothelial cells (HU?VECs). We found that, 1, 10 and 100 μmol/L martentoxin decreased nitric oxide production by HUVECs ex?posed to 10 ng/mL TNF for 6, 12 and 24 hours. We further demonstrated that martentoxin inhibited the activity of iNOS and retarded the down-regulation of eNOS mRNA induced by TNF-α. Therefore, martentoxin could be a potential therapeutic agent for vascular diseases.
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