期刊文献+

Martentoxin对TNF-α引起脐静脉内皮细胞释放一氧化氮的影响

Effects of Buthus Martensii Karsch Toxin Martentoxin in Human Umbilical Vein Endothelial Cells Releasing Nitric Oxide Induced by TNF-α
原文传递
导出
摘要 目的:研究东亚钳蝎毒素Martentoxin对脐静脉内皮细胞释放NO的影响。方法:人脐带经胶原酶消化分离后获得脐静脉内皮细胞,经抗血管性血友病8因子鉴定后,用TNF-α建立NO释放模型,观察Martentoxin对脐静脉内皮细胞释放NO的影响。结果:①经6,12,24h作用后,10μM、100μM Martentoxin能降低TNF-α引起的NO释放增加(P<0.05)。②Martentoxin降低TNF-α引起的iNOS活性增强并对TNF-α引起的内皮源性一氧化氮合酶mRNA下调具有一定保护作用(P<0.05)。结论:Martentoxin抑制TNF-α引起的脐静脉内皮细胞释放NO增加。 Objective: To investigate the impact of Martentoxin on Human umbilical vein endothelial cells (HUVECs) releasing nitric oxide induced by TNF-α. Methods: HUVECs were isolated and identified by tmrnunocytochemistry with Anti-von willebrand Factor (vWF). The NO releasing model of HUVECs was established by treating with 10 ng/ml TNF-α and the effect of Martentoxin on NO releasing was observed. Results: ①Application of 10μM and 100μM Martentoxin inhibits TNF-α-induced NO release after exposure for 6 h, 12 h and 24 h (P〈0.05). ② Martentoxin inhibits the activity ofiNOS and retarded the down-regulation of eNOS mRNA regulated by TNF-α (P〈0.05). Conclusion: Martentoxin inhibits the NO production in HUVECs induced by TNF-α.
出处 《现代生物医学进展》 CAS 2011年第11期2045-2048,共4页 Progress in Modern Biomedicine
关键词 东亚钳蝎 Martentoxin 一氧化氮 脐静脉内皮细胞 BMK Martentoxin Nitric oxide HUVECs
  • 相关文献

参考文献18

  • 1Feng L, Gao R, Gopalakrishnakone P. Isolation and characterization of a hyaluronidase from the venom of Chinese red scorpion Buthus martensi[J]. Comp Biochem Physiol C Toxicol Pharmacol, 2008, 148: 250-257.
  • 2Rodriguez de la Vega RC, Possani LD. Overview of scorpion toxins specific for Na+ channels and related peptides: biodiversity, structure-function relationships and evolution [J]. Toxicon, 2005, 46: 831-844.
  • 3Cao ZY, Shen WQ, Pan YP, et al, Purification, characterization of two peptides from Buthus martensi Karch[J]. J Pept Res, 2003, 62:252-259.
  • 4Wang Y, Chen X, Zhang N, et al. The solution structure of BmTx3B, a member of the scorpion toxin subfamily alpha-KTx 16 [J]. Proteins, 2005, 58:489-497.
  • 5Wang YH, Cao ZY, He WY, et al. 1H-NMR signal assignments and secondary structure analysis of martentoxin [J]. J Asian Nat Prod Res, 2006, 8:511-518.
  • 6Shi J, He HQ, Zhao R, et al. Inhibition of martentoxin on neuronal BK channel subtype (alpha+beta4): implications for a novel interactio~ model [J]. Biophys J, 2008, 94:3706-3713.
  • 7Jaffe EA, Grulich J, Weksler BB, et al. Correlation between thrombin- induced prostacyclin production and inositol trisphosphate and eytoso- lic free calcium levels in cultured human endothelial cells [J]. J Biol Chem, 1987, 262:8557-8565.
  • 8A. Chatterjee, S.M. Black, J.D. Catravas, Endothelial nitric oxide (NO) and its pathophysiologic regulation [J]. Vascul Pharmacol, 2008, 49: 134-140.
  • 9Gao X, Xu X, Belmadani S, et al. TNF-alpha contributes to endotheli- al dysfunction by upregulating arginase in ischemia/reperfusion injury [J]. Arterioscler Thromb Vasc Biol, 2007, 27:1269-1275.
  • 10Medeiros R, Prediger RD, Passos GF, et al. Connecting TNF-alpha signaling pathways to iNOS expression in a mouse model of Alzhei - mer's disease: relevance for the behavioral and synaptic deficits indu- ced by amyloid beta protein[J]. J Neurosci, 2007, 27:5394-5404.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部