肝细胞低密度脂蛋白受体活性对胆汁中胆汁酸影响的实验研究

EFFECT OF LOW DENSITY LIPOPROTEIN RECEPTOR ACTIVITY OF HEPATOCYTE ON BILE ACID DURING GALLSTONE FORMATION ( AN EXPERIMENTAL STUDY )

为研究肝细胞低密度脂蛋白受体对胆汁中胆汁酸的影响及其在胆囊结石过程中可能的机理，采用高胆固醇膳食诱发兔胆囊结石模型，对进食后１、２、３、４周组及对照组动物，采用双波长薄层扫描法测定胆汁中胆汁酸，１２５ＩＬＤＬ放免标记法测定肝细胞低密度脂蛋白受体（ＬＤＬｒ）活性。结果：高胆固醇膳食后２、３、４周组分别有４／１０，６／１０，７／１０出现胆囊结石；胆汁中甘氨胆酸明显降低（Ｐ＜０．０５）；１２５ＩＬＤＬ与肝细胞低密度脂蛋白受体（ＬＤＬｒ）的最大结合力（Ｂｍａｘ）逐渐下降（Ｐ＜０．０５），解离常数（Ｋｄ）值逐渐升高（Ｐ＜０．０５）。上述结果提示：肝细胞低密度脂蛋白受体活性下降，可能导致胆汁中甘氨胆酸减少，致成石性胆汁形成。

To study the mechanism of cholesterol gallstone formation, rabbit models were induced by feeding with high cholesterol diet. Bile acids were tested with biwavelengh thin layer scan and low density lipoprotein receptor activity of hepatocytes binding to 125ILDL were tested with radio immunoassay in different feeding phases as 1,2,3 and 4week groups, as well as the control group. The results showed that cholesterol gallstones in 2,3 and 4week groups were induced in respectively. The contents of glucocholic acid (GCA) in bile were decreased significantly (vs control group, P<0.05). The Bmax values of LDL receptor of hepatocytes binding to 125ILDL were decreased significantly (P<0.05). Kd values of those gradually increased (P<0.05). These suggest that the decreased activity of LDL receptor of hepatocytes would reduce the synthesis of GCA, thus resulting in the formation of cholesterol gallstones.