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作 者:吴志轩 余保平[1] 徐龙[2] 夏虹[1] 罗和生[1]
机构地区:[1]武汉大学人民医院消化内科,湖北武汉430060 [2]南昌大学第一附属医院消化内科,江西南昌330006
出 处:《中国药理学通报》2009年第3期382-385,共4页Chinese Pharmacological Bulletin
基 金:湖北省自然科学基金资助项目(No2006AA412c)
摘 要:目的研究大黄素对豚鼠胆囊肌条收缩及L型钙电流的调节。方法取成年豚鼠,分离胆囊肌条,使用张力传感器记录胆囊肌条的收缩活动。采用酶消化法急性分离豚鼠胆囊平滑肌细胞,使用全细胞膜片钳技术记录L型钙电流。结果预先加入硝苯地平,大黄素对胆囊肌条的收缩效应明显减弱。大黄素增加胆囊平滑肌细胞L型钙电流,呈浓度依赖性。与正常对照组相比,10μmol·L-1大黄素明显增强+10mV时L型钙电流幅度的(45.2±2.26)%(P<0.05)。预先加入PKC抑制剂十字孢碱,大黄素对钙电流的调节基本被抑制。结论大黄素可通过PKC途径增强胆囊平滑肌L型钙电流,从而促进胆囊平滑肌收缩。Aim To on the contraction of SM) and the L-type investigate the effects of emodin gallbladder smooth muscle (GB- calcium current in GBSM cells. Methods Gallbladder muscle strips were obtained from adult guinea pigs and the resting tension was recorded. Gallbladder smooth muscle ceils were isolated by enzymatic digestion, and calcium current was recorded by the whole-cell patch clamp method. Results Emodin-induced contraction of GBSM was significantly attenuated by pretreatment with nifedipine. Emodin increased the L-type calcium current in a dose-dependent manner. When 10umol·L^-1 emodin was applied to GBSM cells, the amplitude of L-type calcium current at + 10 mV was enhanced by (45.2 ± 2. 26)%. In the presence of PKC inhibitor, staurosporine, emodin did not significantly affect the calcium current. Conclusion Emodin enhances L-type calcium current via PKC- dependent pathway and promotes gallbladder contraction.
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