论文部分内容阅读
目的研究脂蛋白脂酶,肝脂酶及载脂蛋白在兔胆囊结石中的变化及作用。方法采用日本杂交大耳兔50只,随机分为对照组,1周组、2周组、3周组和4周组为实验组,实验组饲以1.2%高胆固醇膳食诱以胆囊结石,测定各组脂蛋白脂酶、肝脂酶、血清载脂蛋白和脂质的动态变化,脂蛋白脂酶和肝脂酶采用比色法测定,血清载脂蛋白采用圆周免疫扩散法测定,血清脂质采用酶法测定。结果随着高胆固醇膳食进食时间延长,2周组、3周组和4周组分别有4/10,6/10和7/10只动物出现胆囊结石;肝素化血清中脂蛋白脂酶和肝脂酶活性增加,以3周组和4周组升高明显(与对照组比较,P<0.05);血清载脂蛋白apoB100,apoCⅡ,apoCⅢ明显增加(与对照组比较,P<0.05),apoAI在4周组时降低(与对照组比较,P<0.05);血清总胆固醇,甘油三酯,磷脂,低密度脂蛋白胆固醇和极低密度脂蛋白胆固醇逐渐明显升高(与对照组比较P<0.05),高密度脂蛋白胆固醇及其亚组份有降低趋势,但与对照组比较差异无显著性(P<0.05)。结论高胆固醇膳食后,脂蛋白脂酶和肝脂酶活性增强,血清载脂蛋白和酯质代谢异常变化,促进了胆囊结石形成。
Objective To study the changes and effects of lipoprotein lipase, hepatic lipase and apolipoprotein in rabbit gallbladder stones. Methods Fifty Japanese hybrid rabbits were randomly divided into control group, 1 week group, 2 weeks group, 3 weeks group and 4 weeks group. The experimental group was fed with 1.2% cholesterol diet to induce cholecystolithiasis , The changes of lipoprotein lipase, hepatic lipase, serum apolipoprotein and lipids were measured. The lipoprotein lipase and hepatic lipase were measured by colorimetry, the serum apolipoprotein was determined by immunocytochemistry, the serum Lipid enzymatic assay. Results With the prolongation of hypercholesterolemia diet, gallbladder stones appeared in 4/10, 6/10, and 7/10 animals in the 2nd week, 3rd week and 4th week groups respectively. The levels of lipoprotein lipase and hepatic (P <0.05). Serum apolipoprotein apoB100, apoCⅡ, apoCⅢwere significantly increased (P <0.05 compared with the control group) , ApoAI decreased in the 4-week group (P <0.05 compared with the control group); serum total cholesterol, triglyceride, phospholipid, low-density lipoprotein cholesterol and very low density lipoprotein cholesterol gradually increased (compared with the control Group P <0.05), HDL cholesterol and its subcomponents decreased, but there was no significant difference compared with the control group (P <0.05). Conclusions After hypercholesterolemia, the activity of lipoprotein lipase and hepatic lipase increased, and the changes of serum apolipoprotein and estrogen metabolism changed, which promoted the formation of gallstones.