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作 者:李茜[1] 马会杰[1] 关玥[1] 高璐[1] 张翼[1]
机构地区:[1]河北医科大学基础医学院生理学教研室,河北石家庄050017
出 处:《中国药理学通报》2009年第10期1350-1354,共5页Chinese Pharmacological Bulletin
基 金:河北省科技厅计划资助项目(No07276437)
摘 要:目的观察人参皂苷Rg1对家兔离体小肠平滑肌收缩活动的影响,并探讨其作用机制。方法试验采用经典的离体小肠灌流技术,观察人参皂苷Rg1对家兔小肠平滑肌自发收缩活动的影响,并探讨其作用机制。结果人参皂苷Rg1剂量依赖性的抑制家兔离体小肠平滑肌收缩的幅度;L型钙通道开放剂BayK8644和左旋硝基精氨酸甲酯(L-NAME)均可完全阻断人参皂苷Rg1对家兔小肠平滑肌收缩活动的抑制作用;在无钙台式液中,人参皂苷Rg1抑制rynodine引起的细胞内钙释放所导致的收缩活动。结论人参皂苷Rg1抑制家兔小肠平滑肌的收缩活动,其抑制收缩活动机制可能是:增加小肠平滑肌NO浓度,从而抑制细胞外钙内流和内钙释放。Aim To observe the influences of ginsenoside Rgl on the spontaneous contraction of small intestine smooth muscle of rabbits in vitro and explore the mechanism. Methods With the isothermal perfusion of small intestine in vitro, the influences of ginsenoside Rgl on the spontaneous contraction of small intestine was observed and the mechanism of ginsenoside Rgl was studied. Results Ginsenoside Rgl reduced the amplitude of contraction of small intestine smooth muscle in rabbits in a dose-depended manner. Bay K8644 and nitro-L-arginine methylester ( L-NAME ) could completely block the inhibition of ginsenoside Rgl on the contraction of small intestine smooth muscle. Gin-senoside Rgl inhibited the intracellular calcium-depended contraction induced by rynodine in the Ca2+ free Tyrode's solution. Conclusions Ginsenoside Rgl inhibits the contraction of small intestine smooth muscle of rabbits in vitro. The mechanism may be related to increase NO concentration in small intestine smooth muscle so that it inhibits extracellular Ca2+ inflowing via cell membrane and intracellular Ca2+ releasing via sarcoplasmic reticulum.
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