Myers S I, Turnage R, Kadesky K, Bartula L, Riva A, Kalley-Taylor B
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235, USA.
Prostaglandins. 1995 Jul;50(1):19-32. doi: 10.1016/0090-6980(95)00053-d.
This study examines the hypothesis that PAF stimulates release of PGI2 from inflamed rabbit gallbladder explant cell cultures. New Zealand white rabbits underwent bile duct ligation for 72 h (72 h BDL), or sham operation, Sham and 72 h BDL gallbladder explants were placed in culture, and the cells grown to 75% confluence. The cells were exposed to increasing concentrations of PAF for 60 min. The media analyzed for eicosanoid release by EIA and the cells analyzed for cyclooxygenase and prostacyclin synthase content by immunoblot analysis. PAF increased release of 6-keto-PGF1 alpha from the 72 h BDL gallbladder cell cultures in a dose-related manner which was inhibited by indomethacin preincubation by 90%. The increased 72 h BDL cell release of 6-keto-PGF1 alpha was not associated with changes in the content of cyclooxygenase or prostacyclin synthase. PAF did not alter eicosanoid release from sham control cell cultures. These data suggest that PAF can only up-regulate endogenous 6-keto-PGF1 alpha release from the 72 h BDL cells that had been previously stimulated by inflammation. PAF may thus contribute to gallbladder distention and injury by chronic stimulation of inflamed gallbladder PGI2 release.
本研究检验了血小板活化因子（PAF）刺激炎症状态下兔胆囊外植体细胞培养物释放前列环素（PGI2）这一假说。新西兰白兔接受胆管结扎72小时（72小时胆管结扎，72 h BDL），或接受假手术。将假手术组和72小时胆管结扎组的胆囊外植体进行培养，使细胞生长至75%汇合。将细胞暴露于浓度递增的PAF中60分钟。通过酶免疫分析（EIA）分析培养基中类花生酸的释放情况，通过免疫印迹分析检测细胞中环氧合酶和前列环素合成酶的含量。PAF以剂量相关的方式增加72小时胆管结扎胆囊细胞培养物中6-酮-前列腺素F1α（6-keto-PGF1α）的释放，吲哚美辛预孵育可抑制90%。72小时胆管结扎细胞中6-酮-前列腺素F1α释放增加与环氧合酶或前列环素合成酶含量的变化无关。PAF未改变假手术对照细胞培养物中类花生酸的释放。这些数据表明，PAF只能上调先前受到炎症刺激的72小时胆管结扎细胞内源性6-酮-前列腺素F1α的释放。因此，PAF可能通过慢性刺激炎症胆囊释放PGI2而导致胆囊扩张和损伤。
