Michal Ceregrzyn1, Atsukazu Kuwahara. 1. Laboratory of Physiology, Institute for Environmental Sciences, University of Shizuoka, 52-1 Yada, 422-8526, Shizuoka, Shizuoka, Japan, gpll63@mail.e.u-shizuoka-ken.ac.jp.
Abstract
OBJECTIVES: The epigallocatechin-3-gallate (EGCg) that is present in human diet originates mainly from tea leaves. Catechins have a number of possible application as medicines, however, there is no consistent evidence showing their influence on the gastrointestinal tract. Thus, the aim of the present study was to investigate the effect of EGCg on the motility of the murine isolated intestine. METHODS: Segments of jejunum submerged in Krebs buffer were exposed to EGCg and the response was recorded under isometric conditions. RESULTS: EGCg induced a dose-dependent inhibition of spontaneous activity in the jejunum. EGCg induced a decrease in the amplitude and frequency of jejunal contractions. moreover, the rythmicity of spontaneous, activity was altered in the presence of EGCg. A significant effect of EGCg was observed in the presence of 10(-4) M. The effect of EGCg was in part inhibited by pretreatment with methylene blue (guanylate cyclase inhibitor), while tetrodotoxin, (sodium channel blocker), L-nitro arginine methyl ester (nitric oxide synthase inhibitor), and N-ethylmaleimide (adenylate cyclase inhibitor) showed no effect. CONCLUSIONS: The results of the present study suggest that EGCg inhibits the motility of the jejunum by direct action on smooth muscle cells where a guanylate cyclase-dependent mechanism may be partly involved.
OBJECTIVES: The epigallocatechin-3-gallate (EGCg) that is present in human diet originates mainly from tea leaves. Catechins have a number of possible application as medicines, however, there is no consistent evidence showing their influence on the gastrointestinal tract. Thus, the aim of the present study was to investigate the effect of EGCg on the motility of the murine isolated intestine. METHODS: Segments of jejunum submerged in Krebs buffer were exposed to EGCg and the response was recorded under isometric conditions. RESULTS:EGCg induced a dose-dependent inhibition of spontaneous activity in the jejunum. EGCg induced a decrease in the amplitude and frequency of jejunal contractions. moreover, the rythmicity of spontaneous, activity was altered in the presence of EGCg. A significant effect of EGCg was observed in the presence of 10(-4) M. The effect of EGCg was in part inhibited by pretreatment with methylene blue (guanylate cyclase inhibitor), while tetrodotoxin, (sodium channel blocker), L-nitro arginine methyl ester (nitric oxide synthase inhibitor), and N-ethylmaleimide (adenylate cyclase inhibitor) showed no effect. CONCLUSIONS: The results of the present study suggest that EGCg inhibits the motility of the jejunum by direct action on smooth muscle cells where a guanylate cyclase-dependent mechanism may be partly involved.
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