Key result
Myricetin reduces Kv1.5 channel current by ~64% in HEK293 cells.
Why the study?
The potential effects of myricetin on ion channels, specifically Kv1.5 channels, have remained elusive despite its known anti-arrhythmic effects.
Answers are grounded in this paper and cite their sources.
Myricetin inhibits Kv1.5 channel currents and protein expression in a dose-, time-, and frequency-dependent manner, elucidating a potential mechanism for its anti-arrhythmic effects.
Myricetin (Myr) is a flavonoid that exerts anti-arrhythmic effects. However, its potential effects on ion channels have remained elusive. The aim of the present study was to investigate the effects of Myr on Kv1.5 channels in HEK293 cells. The current of Kv1.5 channels (Ikur) in HEK293 cells was recorded using the whole-cell patch-clamp technique and the expression of the Kv1.5 protein was measured using western blot analysis 24 h after treatment with Myr. The results showed that 5 µM Myr significantly reduced Ikur from 215.04 ± 40.59 to 77.72 ± 17.94 pA/pF (P<0.05; n=5). Myr increased the current suppression from 0 to 0.31 ± 0.12 and 0.55 ± 0.11 over 5 or 20 min, respectively. In addition, Ikur decreased from 376.23 ± 1.30 to 270.19 ± 4.28 pA/pF when the frequency was increased from 0.5 to 4 Hz in HEK293 cells treated with 10 µM Myr for 5 min. Furthermore, Myr reduced hKv1.5 protein expression in a dose-dependent manner. These results demonstrated that Myr inhibited Ikur and the expression of hKv1.5 in HEK293 cells in a dose-, time- and frequency-dependent manner. These observations partly explained the mechanisms by which Myr exerts anti-arrhythmic effect.
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Ou et al. (2015) studied Atrial fibrillation (in vitro model). Myricetin vs. Myr-untreated cells was evaluated on Current of Kv1.5 channels (Ikur) amplitude (p=<0.05). Myricetin at 5 µM significantly reduced the current of Kv1.5 channels (Ikur) in HEK293 cells from 215.04 to 77.72 pA/pF.
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