摘要
目的:建立四氯化碳(CCl4)所致慢性肝损伤、肝硬化大耳白兔模型,在此基础上研究CCl4所致慢性肝损伤的胆囊结石情况,探讨慢性肝损伤家兔胆囊结石形成的机制,从而论证采用慢性肝损伤家兔建立胆石症模型的可行性。方法:将50只家兔随机分成正常组、高胆固醇膳食组、慢性肝损伤组、肝硬化组、肝损伤后胆固醇组。观察家兔的胆石形成情况,透射电镜观察肝细胞超微结构,抽取胆汁细菌培养,酶比色法检测胆囊胆汁中胆汁酸、胆固醇的含量。结果:正常组无一例成石,高胆固醇膳食组8/8成石,慢性肝损伤组5/8成石,肝硬化组6/7成石,肝损伤胆固醇组6/8成石。慢性肝损伤组、肝硬化组、高胆固醇膳食组、肝损伤胆固醇组4组中肝脏超微结构均发生不同程度异常改变,以肝细胞水肿变性、核膜呈锯齿状、粗面内质网增多、线粒体肿胀为多见,肝硬化家兔组可见肝细胞凋亡坏死,高胆固醇膳食组可见胞质中大量脂滴。各组细菌培养均未发现细菌生长。慢性肝损伤组、肝硬化组胆囊胆汁中胆汁酸、胆固醇的含量均较正常组降低。结论:皮下注射CCl4致家兔肝损伤,进而诱导胆囊结石的造模方法可靠。形成的结石为混合性结石。慢性肝病所致肝细胞超微结构异常引起胆汁成分的改变,是肝病患者易发生胆石症的主要原因。慢性肝损伤、肝硬化与胆石症的发生有密切关系,且随着肝脏病变的加重,成石率升高。细菌感染可能不是慢性肝损伤胆囊结石的独立致石因素。
Objective： To discuss the relation that chronic liver injury and cirrhosis caused by carbon tetrachloride（CCl4）. Study the chronic liver injury caused by CCl4 whether could lead to gallstone, which prove the feasibility that build the rabbit model by means of chronic liver injury. Methods： 50 rabbits were divided into 5 groups stochastic. Normal control group, the high cholesterol diet group, the chronic liver injures group, the cirrhosis of liver group, the group that cholesterin calculus after chronic liver injures. We made use of biochemical parameter to observe the changing of bile composition and the functional of liver. We used the light microscope and the electronic microsope to observe the pathological change of the liver hypodermic and the uhrastructure. To observe the rate of gallstone formation, and discuss the influence that the high cholesterol diet to the rate of gallstone formation after liver injury. Results： There was not any gallstone found in the normal control group. Stones were seen in the gallbladder of 8/8 in the high cholesterol diet group, 4/8 in the chronic liver injury group, 6/7 in the liver cirrhosis group, 6/8 in the group that cholesterol calculus after chronic liver injury. The anomaly changes of liver uhrastructure had occurred in all the model group. We could see the hepatocyte hydropic degeneration, the karyotheca change to serration form, the mitochondrion tumefaction, the RER manifold. The hepatocyte turned to apoptosis in the liver cirrhosis group, there were great deal of lipid droplet in cytoplasm in the high cholesterol diet group. The growth of bacteria in the bacterial culture media, was not found The levei of cholesterol and TBA in gall, the chronic liver injury group and liver cirrhosis group were lower than the normal control group. Conclusion： It＇s credible to build the rabbit model that liver injury led to the cholelithiasis by means of hypo CC14. And the property of stone is mixed composition. The change of component of the gall and the decrease of liver function are the primary reason that the cholelithiasis and the hepatic disease are often concurrence. The gallstone is hand in glove with the chronic liver injury and the liver cirrhosis. Rate of the gallstone formation increase as the liver function decrease. Bacterial infection may not be the only factor of the cholelithiasis with chronic liver injurys.
出处
《中国医药导报》
CAS
2007年第12S期106-108,161,共4页
China Medical Herald
基金
广西自然科学基金项目(桂科自0640144)
关键词
慢性肝损伤
胆石症
肝细胞超微结构
动物模型
Chronic liver injures
Cholelithiasis
Ultrastructure of hepatocytes
Animal model
作者简介
通讯作者
