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作 者:吴伟顶[1] 傅华群[1] 邹书兵[1] 黄明文[1] 黄长文[1] 徐艳萍[1]
机构地区:[1]江西医学院第二附属医院肝胆外科研究所,江西南昌330006
出 处:《江西医学院学报》2002年第1期5-7,共3页Acta Academiae Medicinae Jiangxi
基 金:国家自然科学基金资助 (基金编号 3996 0 0 84 )
摘 要:目的 :探讨胆汁胆固醇对胆囊收缩素受体 (CCK R)表达的影响。方法采用放射免疫分析法和受体放射配基结合法检测对照组、高胆固醇组、自然恢复组及治疗组豚鼠门静脉血CCK水平、胆囊CCK R的最大结合容量(Bmax)和亲和力 (Kd) ,同时观察空腹胆囊体积 (FV)、胆囊胆汁量 (FB)和餐后胆囊体积 (RV)、胆囊胆汁量 (RB)及胆囊收缩率 (E % )、胆汁胆固醇浓度的变化。结果与对照组比较 ,高胆固醇组豚鼠FV、FB增大 (P <0 .0 5 ) ,RV、RB也增大 ,胆囊收缩率下降 (P <0 .0 1) ,胆汁胆固醇浓度升高 (P <0 .0 5 ) ,门静脉血CCK水平及CCK R的Kd无改变 ,而CCK R的Bmax下降 (P <0 .0 1) ;治疗组上述各项指标正常。结论胆汁中的高胆固醇通过下调胆囊CCK R表达而导致胆囊收缩功能障碍 。Objective: To explore the effect of cholesterol of bile on Cholecystokinin receptor (CCK R) of the gallbladder. Methods: Serum Cholecystokinin (CCK) level in portal vein, maximal binding capacity (Bmax), and Kd of CCK R in the gallbladder were measured in four groups of guniea pigs by RIA and RBA. Meanwhile the concentration of cholesterol in bile was also observed.Results:Compared with control group, after two weeks of high cholesterol feeding, there were declines in both gallbladder contraction rate( P <0.05) and Bmax of CCK R( P <0.01). In contrast, there was elevation in fasting gallbladder volume (FV) and concentration of cholesterol in bile( P <0.05) without any changes of serum CCK level and Kd of CCK R.The changes induced by high cholesterol feeding were reversed to normal levels in treated group.Conclusion:A high level of cholesterol in the gallbladder bile results in a defective muscle contraction by down regulating CCK R in the gallbladder. As a result, the reduction of cholesterol concentration of bile can result in the preservation of gallbladder contraction.
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