摘要
目的 探讨 CCK引起兔 Oddi括约肌细胞收缩的钙动员机制 .方法 取新西兰兔 Oddi肌组织 ,进行原代细胞培养 .将培养的 4- 7代细胞行 Fluo- 3/AM负载 ,用激光共聚焦显微镜测量不同拮抗剂对 CCK诱导的细胞内 Ca2 +增加的影响 .结果 不加拮抗剂 10 - 7m ol· L- 1 CCK使细胞内 Ca2 +增加 (130± 43) %,用 EGTA+维拉帕米阻断细胞外钙离子内流时 ,CCK诱导细胞 Ca2 +增加 (10 4± 2 3) %,而用肝素时细胞内Ca2 +增加值为 (2 3± 19) %,加入普鲁卡因后细胞内 Ca2 +增加(85± 37) %.同其他组对比 ,肝素明显抑制了 CCK诱导的Ca2 +升高 (P<0 .0 1) .结论 CCK通过动员细胞内 IP3 敏感钙库的钙离子引起 Oddi细胞 Ca2 +升高 。
AIM To demonstrate the mechanism of the calcium mobilization pathway in rabbit Okki's sphincter muscle cells induced by cholecystokinin (CCK). METHODS Rabbit Oddi's sphincter muscle cells was cultured and loaded with Ca 2+ indicator fluo 3/AM, then CCK induced intraqcellular Ca 2+ Increase was measured under cofocal microscope after adding the different antagonists. RESULTS CCK (10 -7 mol·L -1 ) induced intracellular calcium increase was (130±43)%, and it decreased to (104±23)% after extracellular calcium eliminated by EGTA and verapamil. After antagonists heparin and procaine were added, it further decreased to (23±19)% and (85±37)% respectively. Compared with other proups, CCK induced intracellular Ca 2+ increase was sharply inhibited by heparin ( P <0.01). CONCLUSION Intracellular calcium increase of SO cells elicited by CCK is predominantly mobilized through IP3 sensitive pathwas, and could be inhibited by incubation with heparin.
出处
《第四军医大学学报》
北大核心
2001年第22期2064-2067,共4页
Journal of the Fourth Military Medical University
