CAJ | 학술논문

目的探讨骨桥蛋白在人胆固醇结石形成中的作用.方法 36例胆固醇结石患者为结石组,19例肝移植供体为正常组,分别测定骨桥蛋白、钙离子及脂质成分在胆囊胆汁中的含量,用成核时间法研究骨桥蛋白在胆汁中的成核作用.结果骨桥蛋白呈剂量依赖性地抑制胆固醇自发成核.50 μg/ml的骨桥蛋白可分别使结石组和正常组胆汁的成核时间延缓48.90％和17.07％,100 μg/ml的骨桥蛋白可使成核时间延缓91.51％和32.93％;并可抑制钙离子诱导的促成核作用.50μg/ml骨桥蛋白+钙离子可分别使结石组和正常组胆汁成核时间延缓75.78％和33.96％,而100μg/ml骨桥蛋白+钙离子则使成核时间分别延缓125.90％和62.26％.结石组胆汁中胆固醇、磷脂、胆汁酸及胆固醇饱和指数均显著高于正常组胆汁(P＜0.05),而骨桥蛋白和钙离子含量则明显低于正常组胆汁中的含量(P＜0.05).结论骨桥蛋白可抑制胆固醇成核,并参与胆结石的发生发展.
목적 탐토골교단백재인담고순결석형성중적작용.방법 36례담고순결석환자위결석조,19례간이식공체위정상조,분별측정골교단백、개리자급지질성분재담낭담즙중적함량,용성핵시간법연구골교단백재담즙중적성핵작용.결과 골교단백정제량의뢰성지억제담고순자발성핵.50 μg/ml적골교단백가분별사결석조화정상조담즙적성핵시간연완48.90％화17.07％,100 μg/ml적골교단백가사성핵시간연완91.51％화32.93％;병가억제개리자유도적촉성핵작용.50μg/ml골교단백+개리자가분별사결석조화정상조담즙성핵시간연완75.78％화33.96％,이100μg/ml골교단백+개리자칙사성핵시간분별연완125.90％화62.26％.결석조담즙중담고순、린지、담즙산급담고순포화지수균현저고우정상조담즙(P＜0.05),이골교단백화개리자함량칙명현저우정상조담즙중적함량(P＜0.05).결론 골교단백가억제담고순성핵,병삼여담결석적발생발전.
Objective To investigate the role of osteopontin (OPN) in cholesterol gallstone formation.Methods Gallbladder bile was obtained from patients with cholelithiasis (n=36,the experimental group) and from donors of liver transplantation (n=19,the control group).OPN,calcium ion and lipid were analysed quantitively.The nucleating role of OPN in bile was evaluated using nucleating time (NT) approach.Results OPN inhibited cholesterol nucleation in a dose dependent manner.OPN (50 μg/ml and 100 μg/ml) prolonged NT by 48.90％ (91.51％) and 17.07％ (32.93％) in lithogenic and control bile,respectively.OPN (100 μg/ml) also inhibited the nucleating effect induced by calcium ion.Furthermore,a combination of OPN (50 μg/ml) and calcium prolonged NT by 75.78％ and 33.96％ in lithogenic and control bile,respectively.A combination of OPN (100 μg/ml) and calcium prolonged NT by 125.9％ and 62.26％ in the 2 groups.The contents of osteopontin and calcium were significantly lower in lithogenic bile than control bile (P＜0.05).On the other hand,the cholesterol saturation index and the contents of cholesterol,phospholipid and bile acid were significantly higher (P＜0.05).Conclusions OPN inhibited cholesterol gallstone formation.It may be involved in the pathogenesis of cholelithiasis.