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刀豆蛋白A与四氯化碳诱导的小鼠急性肝损伤病理特点 被引量:2

Study on the pathological features of acute liver injury induced by concanavalin A and carbon tetrachloride in mice
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摘要 目的对比刀豆蛋白A(Con A)与四氯化碳(CCl_4)诱导的小鼠(C57BL/6)急性肝损伤病理形态特点的异同。方法 Con A(Sigma公司)10 mg/kg尾静脉注射一次;腹腔注射10%CCl_4油剂0.1 ml/10 g一次,24 h取肝脏4%中性福尔马林固定,苏木精-伊红染色(HE),显微镜下观察病理形态。结果 Con A损伤组:肝细胞凝固性坏死并未使肝腺泡III带的肝细胞完全破坏,部分肝细胞保留,中央静脉保留,坏死带亦可出现在肝腺泡I带,大部肝细胞轮廓可见;CCl_4损伤组:肝小叶中心(肝腺泡III带)凝固性坏死,肝细胞崩解,细胞核崩解。坏死范围大者可累及肝腺泡II带,坏死带与毗邻小叶坏死带相连成片。经图像分析比较发现,Con A模型组较CCl_4组大鼠坏死面积范围小,差异有统计学意义(12.5%vs.25.2%,P<0.05)。结论 Con A与CCl_4诱导的急性肝损伤机制不同,病理形态学变化不同,坏死面积也不同。了解二者的区别可以更好地利用两种动物模型,筛选有效的治疗方案。 Objectiye To compare the pathological features of acute liver injury caused by concanavalin A(Con A)and carbon tetrachlo-ride(CCl4)in C57BL/ 6 mice. Methods Con A(10 mg/ kg)was injected via tail vein of mice and CCl4(10% ,0. 1 ml/ kg)was administered by intraperitoneal injection to mice. There were 6 mice in control group,7 mice in Con A group and 7 mice in CCl4 group. Livers of mice were harvested after 24 hours and fixed in 4% neutral formalin,then stained by hematoxylin - eosin for morphological observation. Results In mice models of Con A group,coagulative necrosis occurred both in band I and band III of hepatic acinus. Furthermore,hepatocytes were not entirely ne-crosed and cell membrane of hepatocytes had been preserved. On the contrary,in CCl4 models,necrosis occurred universally in band III of hepatic acinus,and hepatocytes were entirely died. Necrotic area in Con A model was significantly lesser than that of CCl4 model(12. 5% vs. 25. 2% , P 〈 0. 05). Conclusion Due to the difference in mechanism of liver injury,pathological features of acute liver injury caused by Con A or CCl are different;hence the strategy for treatment is also different. The understanding of this point of view can help investigators to select the appropri-ate models for screening effective medication.
出处 《临床和实验医学杂志》 2016年第16期1553-1555,共3页 Journal of Clinical and Experimental Medicine
基金 北京市高层次技术人才学科骨干项目资助(2013-3-069)
关键词 小鼠 急性肝损伤 刀豆蛋白A 四氯化碳 病理特点 Acute hepatic injury Concanavalin A Carbon tetrachloride Pathological feature
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  • 1Xiao-Wen Li, Rong Zhu,Bo Li,Mei Zhou,Qing-Jian Sheng,Ye-Peng Yang,Nan-Yin Han,Zai-Quan Li.Mechanism underlying carbon tetrachloride-inhibited protein synthesis in liver[J].World Journal of Gastroenterology,2010,16(31):3950-3956. 被引量:4
  • 2Lei Yang Yong-feng Liu Shu-rong Liu Gang Wu Jia-lin Zhang Yi-man Meng Shao-wei Shong Gui-chen Li.PREVENTION AND TREATMENT OF REJECTION AFTER SIMULTANEOUS PANCREAS-KIDNEY TRANSPLANTATION[J].Chinese Medical Sciences Journal,2005,20(3):210-213. 被引量:3
  • 3胡水清,黄依雯,秦伟,柳娟,徐辰迪,孔方圆,张雁云.ConA诱导小鼠肝损伤模型的发病机制[J].中国血液流变学杂志,2007,17(1):159-162. 被引量:30
  • 4Friedman SL. Liver fibrosis -- from bench to bedside [ J]. J Hepa- tol, 2003,38( Suppl 1 ) :S38-S53.
  • 5Hemandez-Gea V, Friedman SL. Pathogenesis of liver fibrosis [ J ]. Annu Rev Pathol, 2011, ( 6 ) :425-456.
  • 6Bouillon R. Genetic and environmental determinants of vitamin D status [J]. Lancet, 2010,376(9736):148-149.
  • 7Kitson MT, Roberts SK. D-livering the message: the importance of vitamin D status in chronic liver disease [ J]. J Hepatol, 2012, 57(4) :897-909.
  • 8Ramirez AM, Wongtrakool C, Welch T, et al. Vitamin D inhibi- tion of pro-fibrotic effects of transforming growth factor betal in lung fibroblasts and epithelial cells [ J ]. J Steroid Biochem Mol Biol, 2010,118(3) :142-150.
  • 9Zhang Y, Kong J, Deb DK, et al. Vitamin D receptor attenuates renal fibrosis by suppressing the renin-angiotensin system[J]. J Am Soc Nephrol, 2010,21 (6) :966-973.
  • 10Weber LW, Boll M, Stampfl A. Hepatotoxicity and mechanism of action of haloalkanes : carbon tetrachloride as a toxicological model [ J]. Crit Rev Toxicol, 2003,33(2) :105-136.

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