Objective · To investigate the effect of resveratrol (Res) on colonic movement in mice and its mechanism. Methods · The effects of Res (10, 20, 40, and 80 μmol/L) on spontaneous contraction of colonic smooth muscle in mice and colonic migrating motor complex (CMMC) were recordedusing a multi-channel physiological recorder. Colonic smooth muscle strips were pretreated with the following tool medicines: BayK8644 (an activator of L-type Ca2+ channel), TEA (tetraethylammonium, a non-selective K+ channel blocker), TTX (tetrodotoxin, a Na+ channel blocker), atropine (a cholinergic neuron inhibitor), L-NAME [Nω-nitro-L-arginine methyl ester, a nitric oxide (NO) synthase inhibitor], NPPB[5-nitro-2-(3-phenylpropylamino) benzoic acid, an ANO1 (anoctamin 1) channel inhibitor] and apamin [a small conductance Ca2+-activated K+ channel 3 (SK3) channel inhibitor].elution, the effects of Res on spontaneous contraction of colonic smooth muscle strips before and after pretreatment were recorded and compared. Finally, the effect of Res on L-type Ca2+ channel currents were recordedusing the whole-cell patch clamp technique in freshly dispersed colonic smooth muscle cells. Results · Res significantly inhibited colonic smooth muscle spontaneous contraction in a dose-dependent manner and markedly decreased CMMC in the proximal and the distal colon. BayK8644 significantly blocked the Res-induced inhibition. Besides, Res dramatically inhibited L-type Ca2+ channel currents in colonic smooth muscle cells. However, TEA did not block the inhibitory effect of Res. In addition, TTX, atropine, L-NAME, NPPB and apamin had no effect on the inhibitory effect of Res on spontaneous contraction of colonic smooth muscle. Conclusion · Res inhibits colonic movement via inhibiting L-type Ca2+ channel in mice, and its mechanism may be irrelevant to potassium channel, the enteric nervous system, NO and interstitial cell.