脂多糖联合D.docVIP

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 翟亚南，王晶晶，李梦，池亚菲，孟霞，彭博雅，焦昆，卢静 (首都医科大学,北京，100069) 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 30mg/mL D-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。 关键词： D-氨基半乳糖；脂多糖；肝损伤；动物模型 Chronic hepatic injury modeling in mice induced by D–galactosamine and lipopolysaccharide combination ZHAI Ya-nan,WANG Jing-jing,LI Meng,CHI Ya-fei,MENG Xia,PENG Bo-ya,JIAO Kun,LU Jing (Capital Medical University,Beijing,100069,China) 【Objective】Objective: To research the method of Chronic hepatic injury modeling in mice induced by D–galactosamine and lipopolysaccharide combination. Methods:Injected D–galactosamine(30mg/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. 【】 D – galactosamine ; ipopolysaccharide;Hepatic injury; Animal Models 肝脏疾病是人类最常见的疾病之一, 严重威胁着人类健康。为此,研发抗肝脏疾病的有效药物显得尤为重要。动物实验是药物进入临床的必经之路,在研发抗肝脏疾病药物过程中,选择有科学性、实用性、重现性的肝损伤动物模型的意义十分重要[1]。目前，有很多药物模型，重复性和模拟性好的药物毒性大，建模结果不够稳定。D-[2]。为此,本实验就以D-氨基半乳糖联合脂多糖（以下简称D+L）致小鼠慢性肝损伤模型的制备进行探讨。 1材料与方法 1.1实验动物: SPF级健康雄性BALB/ c小鼠22只，体重18-22g，购于北京维通利华实验动物科学技术有限公司【SCXK(京)2012-0001】。在首都医科大学实验动物部屏障环境开展实验【SYXK(京)2010-0020】。室温20-25 ℃, 相对湿度40%-70%。小鼠分笼饲养, 每笼饲养3-4只，给予自由进食和饮水，饲料和饮水均经灭菌处理。 1.2试剂与仪器：D-氨基半乳糖（NanjingBoyuanPharmatechCo.,Ltd、脂多糖（美国Sigma