期刊文献+

Expression of nitric oxide synthase in T-cell-dependent liver injury initiated by ConA in Kunming mice 被引量:1

Expression of nitric oxide synthase in T-cell-dependent liver injury initiated by ConA in Kunming mice
下载PDF
导出
摘要 Objective: To investigate whether nitric oxide synthase (NOS) is expressed in T-cell-dependent liver injury initiated by concanavalin A (ConA) in Kunming mice and study the possible effect of nitric oxide(NO) on liver injury models. Methods: Liver injury in Kunming mice was induced by administration of ConA through tail vein. Expression of NOS in the liver was detected by NADPH diaphorase staining method. The possible effect of NO on liver injury models was obtained by L-NAME injection to suppress synthesis of NO. Results: NOS has a strong expression in hepatocytes after ConA injection, especially in those close to the central vein, while only a weak expression was found in the epithelial cells in control group. Liver injury became more serious when NO synthesis was inhibited by L-NAME, accompanied by great malondialdehyde(MDA) increase in serum and severe intrahepatic vascular thrombosis. Conclusion: NOS markedly expressed in ConA-induced liver injury, which may subsequently promote nitric oxide synthesis. Increasement of nitric oxide has a protective effect on ConA-induced liver injury. Objective: To investigate whether nitric oxide synthase (NOS) is expressed in T-cell-dependent liver injury initiated by concanavalin A (ConA) in Kunming mice and study the possible effect of nitric oxide(NO) on liver injury models. Methods: Liver injury in Kunming mice was induced by administration of ConA through tail vein. Expression of NOS in the liver was detected by NADPH diaphorase staining method. The possible effect of NO on liver injury models was obtained by L-NAME injection to suppress synthesis of NO. Results: NOS has a strong expression in hepatocytes after ConA injection, especially in those close to the central vein, while only a weak expression was found in the epithelial cells in control group. Liver injury became more serious when NO synthesis was inhibited by L-NAME, accompanied by great malondialdehyde(MDA) increase in serum and severe intrahepatic vascular thrombosis. Conclusion: NOS markedly expressed in ConA-induced liver injury, which may subsequently promote nitric oxide synthesis. Increasement of nitric oxide has a protective effect on ConA-induced liver injury.
出处 《Journal of Medical Colleges of PLA(China)》 CAS 2004年第2期112-114,共3页 中国人民解放军军医大学学报(英文版)
关键词 nitric oxide synthase nitric oxide concanavalin A liver injury 一氧化氮合酶 T细胞相关性肝损伤 动物模型 刀豆体球蛋白A 病理学
  • 相关文献

参考文献13

  • 1[1]Kimura K, Ando K, Ohnishi H et al. hmmtunopathogenesis of hepatic fibrosis in chronic liver injury induced by repeatedly administered concanavalin A[J]. Int Immunol, 1999; 11(9): 1491.
  • 2[2]Sakamoto T, Ezure T, Lunz J et al. Concanavalin A simultaneously primes liver hematopoietic and epithelial progenitor cells for parallel expansion during liver regeneration after partial hepatectomy in mice [J]. Hepatology,2000; 32(2): 256.
  • 3[3]Shirin H, Dotan I, Papa M et al. Inhibition of concanavalin A-induced acute T cell dependent hepatic damage in mice by hypothyroidism[J]. Liver, 1999; 19(3): 206.
  • 4[4]Cao Q, Batey R, Pang G et al. Ethanol-altered liver-associated T cells mediate liver injury in rats administered Concanavalin A (Con A) or lipopolysaccharide (LPS) [J]. Alcohol Clin Exp Res, 1999; 23(10): 1660.
  • 5[5]Fiorucci S, Santucci L, Antonelli E et al. NO-aspirin protects from T cellmediated liver injury by inhibiting caspase-dependent processing of Th1-like cytokines[J]. Gastroenterology, 2000; 118(2): 404.
  • 6[6]Okamoto T, Nakano Y, Asakura W et al. Expression of cytokine mRNA in extrahepatic organs in a mouse concanavalin A-hepatitis model [J]. Jpn J Pharmacol, 1998; 77(3): 219.
  • 7[7]Bozza M, Bliss JL, Maylor R et al. Interleukin-11 reduces T-cell-dependent experimental liver injury in mice[J]. Hepatology, 1999; 30(6):1441.
  • 8[8]Sass G, Koerber K, Bang R et al. Inducible nitric oxide synthase is critical for immune-mediated liver injury in mice[J]. J Clin Invest, 2001; 107(4): 439.
  • 9[9]Kunstle G, Hentze H, Germann PG et al. Concanavalin A hepatotoxicity in mice: tumor necrosis factor-mediated organ failure independent of caspase-3-1ike protease activation[J]. Hepatology, 1999; 30(5): 1241.
  • 10[10]Nanji AA, Greenberg SS, Tahan SR et al. Nitric oxide production in experimental alcoholic liver disease in the rat: role in protection from injury [J]. Gastroenterology, 1995; 109(3): 899.

同被引文献4

引证文献1

二级引证文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部