@article{APS7645,
author = {Li-Zan Wang and Qing-Zhu Zhang and Xiu-Zhou Hu and Ning Lun and Fan-He Zhu},
title = {Verapamil, cyproheptadine, and anisodamine antagonized [Ca2+]i elevation induced by TNFalpha in a single endothelial cell},
journal = {Acta Pharmacologica Sinica},
volume = {22},
number = {10},
year = {2016},
keywords = {},
abstract = {Aim: To study the effect of tumor necrosis factor alpha (TNFalpha) on intracellular free Ca2+ concentration ([Ca2+]i) and the effects of verapamil (Ver), cyproheptadine (Cyp), and anisodamine (Ani) on TNFalpha-induced [Ca2+]i changes in single endothelial cell, and to explore the mechanisms of TNFalpha-mediated shock and antishock actions of Cyp and Ani.
Methods: Human umbilical vein endothelial cell strains (ECV304) were seeded in 35-mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca2+]i in single endothelial cell were determined by laser scanning confocal microscopy.
Results: After stimulation with TNFalpha, [Ca2+]i in single endothelial cell rapidly increased in a concentration-dependent manner and arrived at the peak value within 60 s, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca2+]i elevation was more obvious in nuclear than in cytoplasma and decreased slowly. Ver (1, 2 micromol/L), Cyp (30, 60 micromol/L), and Ani (20, 40 micromol/L) markedly inhibited TNFalpha 1.2 nmol/L-induced [Ca2+]i elevation.
Conclusion: TNFalpha markedly induces elevation of [Ca2+]i in a single endothelial cell, it may be an important mechanism of TNFalpha-induced shock and tissue injury. That Cyp and Ani obviously suppress TNFalpha-induced [Ca2+]i elevation probably is one of the mechanisms of their antishock effects.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/7645}
}