ArticleWorld journal of gastroenterology2003
Effects of tetrandrine on calcium and potassium currents in isolated rat hepatocytes.
Article in World journal of gastroenterology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Tetrandrine Suppresses Transient Receptor Potential Cation Channel Protein 6 Overexpression- Induced Podocyte Damage via Blockage of RhoA/ROCK1 Signaling.Drug design, development and therapy · 2020Article
- Design, synthesis and bioactivity investigation of tetrandrine derivatives as potential anti-cancer agents.MedChemComm · 2018Article
- Inhibitory effects of tetrandrine on the Na(+) channel of human atrial fibrillation myocardium.Acta pharmacologica Sinica · 2009Article
- Hydrogen peroxide mobilizes Ca2+ through two distinct mechanisms in rat hepatocytes.Acta pharmacologica Sinica · 2009Article
- Electrophysiological effects of anthopleurin-Q on rat hepatocytes.World journal of gastroenterology · 2004Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the effects of tetrandrine (Tet) on calcium release-activated calcium current (I(CRAC)), delayed rectifier potassium current (I(K)), and inward rectifier potassium currents (I(K1)) in isolated rat hepatocytes.
methodsHepatocytes of rat were isolated by using perfusion method. Whole cell patch-clamp techniques were used in our experiment.
resultsThe peak amplitude of I(CRAC) was -508+/-115 pA (n=15), its reversal potential of I(CRAC) was about 0 mV. At the potential of -100 mV, Tet inhibited the peak amplitude of I(CRAC) from -521+/-95 pA to -338+/-85 pA (P<0.01 vs control, n=5), with the inhibitory rate of 35 % at 10 micromol/L and from -504+/-87 pA to -247+/-82 pA (P<0.01 vs control, n=5), with the inhibitory rate of 49 % at 100 micromol/L, without affecting its reversal potential. The amplitude of I(CRAC) was dependent on extracellular Ca(2+) concentration. The peak amplitude of I(CRAC) was -205+/-105 pA (n=3) in tyrode's solution with Ca(2+) 1.8 mmol/L (P<0.01 vs the peak amplitude of I(CRAC) in external solution with Ca(2+) 10 mmol/L). Tet at the concentration of 10 and 100 micromol/L did not markedly change the peak amplitude of delayed rectifier potassium current and inward rectifier potassium current (P>0.05 vs control).
conclusionTet protects hepatocytes by inhibiting I(CRAC), which is not related to I(K) and I(K1).
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