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Luteolin suppresses colonic smooth muscle motility via inhibiting L-type calcium channel currents in mice
Author(s) -
Meng Yang,
Yang Zhou,
Leilei Wan,
Jianzhong Ye,
Hsin-I Lu,
Xu Huang,
Wen-Xie Xu
Publication year - 2020
Publication title -
general physiology and biophysics
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.376
H-Index - 39
eISSN - 1338-4325
pISSN - 0231-5882
DOI - 10.4149/gpb_2019045
Subject(s) - luteolin , apamin , channel blocker , potassium channel , motility , chemistry , pharmacology , potassium channel blocker , patch clamp , calcium channel blocker , charybdotoxin , calcium channel , calcium activated potassium channel , biophysics , calcium , biochemistry , receptor , medicine , biology , microbiology and biotechnology , antioxidant , organic chemistry , quercetin
As a naturally occurring flavone, luteolin has received much attention due to its antioxidant, anti-inflammatory and anticancer functions. In the present study, we investigated the effect of luteolin on colonic motility and its mechanism using isometric muscle recording and the whole-cell patch-clamp technique in mice. Luteolin dose-dependently inhibited colonic smooth muscles motility and CMMC significantly. BayK8644, an L-type Ca2+ channel agonist, significantly attenuated the luteolin-induced inhibition. Moreover, the calcium currents recorded in colonic smooth muscle cells were dramatically inhibited by luteolin. However, no significant changes were found in the luteolin-induced inhibitory effect in the presence of TEA, a nonselective K+ channel blocker, glibenclamide, an ATP-dependent K+ channel blocker, and apamin, a small-conductance Ca2+-activated K+ channel blocker. Additionally, luteolin did not affect potassium currents. Furthermore, TTX, a Na+ channel blocker, L-NAME, an inhibitor of nitric oxide (NO) synthase, ODQ, an inhibitor of NO-sensitive guanylyl cyclase, and Ani9, a specific ANO1 channels blocker, had no effect on the luteolin-induced suppression. These results suggest that luteolin inhibited colonic smooth muscle motility by inhibiting L-type calcium channels in mice but not through potassium channels, the enteric nervous system (ENS), NO signaling pathways or ANO1 channels of interstitial cells of Cajal (ICCs).

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