D-氨基半乳糖联合脂多糖诱导小鼠慢性肝损伤模型的建立  被引量:8

Chronic hepatic injury modeling in mice induced by D – galactosamine and lipopolysaccharide combination

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作  者:翟亚南[1] 王晶晶[1] 李梦[1] 池亚菲[1] 孟霞[1] 彭博雅[1] 焦昆[1] 卢静[1] 

机构地区:[1]首都医科大学,北京100069

出  处:《中国比较医学杂志》2014年第5期62-65,F0004,共5页Chinese Journal of Comparative Medicine

基  金:2010年度北京市属高等学校人才强教深化计划中青年骨干人才(PHR201008390)

摘  要:目的研究D-氨基半乳糖联合脂多糖诱导小鼠慢性肝损伤模型建立的方法。方法 30 mg/mLD-氨基半乳糖和2μg/mL脂多糖混合溶液,腹腔注射,每2天1次,连续8周。监测小鼠饮食和体重变化;取血测定小鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平;取肝组织,HE和Masson染色,观察小鼠肝组织结构、细胞形态及纤维化程度。结果模型组ALT水平升高,肝细胞变性、坏死等病变,组织纤维化明显增生。结论 D-氨基半乳糖联合脂多糖可诱导小鼠的慢性肝损伤模型。Objective To research the method of Chronic hepatic injury modeling in mice induced by D -galactosamine and lipopolysaccharide combination . Methods Injected D-galactosamine ( 30 mg/mL ) and lipopolysaccharide ( 2μg/mL ) combination by intraperitoneal injection , two days at a time for 8 weeks .Monitored variation of diet and weight; detected serum level of alanine aminotransferase ( ALT ) and aspartate aminotransferase (AST), been put to death in mice and removed the liver tissue .strained hepatic tissue by the HE and Masoon dye to observe Liver tissue structure and cellular morphology and the degree of fibrosis .Results Lipopolysaccharide and D-galactosamine combination resulted in ALT rise , hepatocyte degeneration and necrosis ,collagen fiber hyperplasia obviously . Conclusion D-galactosamine and Lipopolysaccharide combination could induce mice chronic hepatic injury modeling .

关 键 词:D-氨基半乳糖 脂多糖 肝损伤 模型 动物 

分 类 号:R332[医药卫生—人体生理学]

 

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