ArticleJournal of biomedical research2013
Martentoxin, a large-conductance Ca(2+)-activated K(+) channel inhibitor, attenuated TNF-α-induced nitric oxide release by human umbilical vein endothelial cells.
Article in Journal of biomedical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Scorpion (Buthus martensii Karsch) in Chinese medicine: a review of traditional uses, chemical constituents, pharmacology, and toxicology.Frontiers in pharmacology · 2025Review
- The Significant Therapeutic Effects of Chinese Scorpion: Modern Scientific Exploration of Ion Channels.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Andrographolide inhibits nuclear factor-κB activation through JNK-Akt-p65 signaling cascade in tumor necrosis factor-α-stimulated vascular smooth muscle cells.TheScientificWorldJournal · 2014Article
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Authors and funding
7 authors.
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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 Ca(2+)-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 (HUVECs). We found that, 1, 10 and 100 µmol/L martentoxin decreased nitric oxide production by HUVECs exposed 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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