>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
大鼠急性坏死性胰腺炎时P物质在肠壁上的表达及其与肠黏膜通透性的关系
作者:宿士智1 石欣2 高乃荣2 
单位:1.北京市大兴区医院,普外科,北京,102600; 2.东南大学附属中大医院,普外科,江苏,南京,210009
关键词:急性坏死性胰腺炎 神经激肽-1受体 P物质 肠黏膜通透性 大鼠 
分类号:R657.51
出版年·卷·期(页码):2005·24·第六期(359-363)
摘要:

目的:了解急性坏死性胰腺炎(ANP)时大鼠回肠组织中P物质的表达及其与肠黏膜通透性的关系.方法:健康成年SD大鼠随机分为对照组40只和ANP组40只,对照组开腹后只翻动胰腺,ANP组大鼠胰胆管恒速逆行注射5%牛黄胆酸钠制成ANP大鼠模型,分别于制模成功后8、12、16和20h处死大鼠采取标本.用同位素法测定肠黏膜通透性,免疫组织化学方法检测P物质在回肠组织中的表达水平和组织学定位.结果:ANP组大鼠回肠组织中P物质的表达以及肠黏膜通透性(99mTc-DTPA排泄率)较对照组明显增加(P<0.05).P物质在回肠组织中的表达与肠黏膜通透性呈明显正相关(r=0.66,P<0.01).结论:ANP时大鼠回肠组织中P物质表达升高,且随时间延长而增加,其表达与大鼠肠黏膜通透性呈正相关.

Objective To investigate the expression of substance P in rats’ intestinal tissue and study the relation between substance P and mucosa permeability in acute necrotizing pancreatitis(ANP).Methods 80 adult Sprague-Dawley rats were randomly divided into control group((n=)40) and ANP group((n=)40).Sacrifices were made in 8,12,16 and 20?h later in every group after ANP model was established by injecting 5% sodium taurocholate into pancreatic duct respectively.The intestinal mucosal permeability and the expression of substance P were studied.Results In ANP groups,intestinal mucosal permeability and the expression of substance P were significantly higher than those in the control group((P<)0.05).The overexpression of substance P was correlated with the intestinal mucosal permeability in ANP(r=0.66,P<(0.01)).Conclusion The expression of substance P and the permeability in intestine of rats are increased significantly in ANP.There exists a possitive correlation between substance P and the intestinal permeability.

参考文献:

[1] BHATIA M, NEOPTOLEMOS J P, SLAVIN J. Inflammatory mediators as therapeutic targets in acute pancreatitis, 2001(4)
[2] MARDARA J L. Pathobiology of the intestinal epithelial barrier, 1990(6)
[3] HULST R R, MEYENFELDT M F, KREEL B K. Gut permeability,intestinal morphology,and nutrition depletion. 1998(1). doi:10.1016/S0899-9007(97)00385-7
[4] APPELGREN A, APPELGREN B, KOPP S. Substance Passociated increase of intra-articular temperature and pain threshold in the arthritic TMJ, 1998(2)
[5] BORSON D B, BROKAW J J, SEKIZAWA K. Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections, 1989(16)
[6] GRADY E F, YOSHIMI S K, MAA J. Substance P mediates inflammatory edema in acute pancreatitis via activation of the neurokinin-1 receptor in rats and mice. 2000(3). doi:10.1038/sj.bjp.0703343
[7] MAA J, GRADY E F, KIM E H. NK1 receptor desensitization and neutral endopeptidase terminate SP-induced pancreatic plasma extravasation, 2000(4)
[8] 石欣, 高乃荣, 霍明东. P物质受体在急性出血坏死性胰腺炎肺组织中的过度表达. 江苏医药2003(1). doi:10.3969/j.issn.0253-3685.2003.01.005
[9] SHI X, GAO N R, GUO Q M. Relationship between overexpression of NK-1R,NK-2R and intestinal mucosal damage in acute necrotizing pancreatitis. World J Gastroenterol2003(1)
[10] 石欣, 高乃荣, 杨永久. 急性坏死性胰腺炎肠黏膜损害与NK-1R的过度表达相关. 中国病理生理杂志2003(8). doi:10.3760/cma.j.issn.1674-1935.2003.z1.029
[11] BLUM A M, METWALI A, ELLIOT D. Substance P receptor antagonist inhibits murine IgM expression in developing schistosome granulomas by blocking the terminal differentiation of intragrantdoma B cells, 1996(1-2)
[12] DICKERSON C, UNDEM B, BULLOCK B. Neuropeptide regulation of proinflammatory cytokine responses, 1998(5)
[13] COCCHIARA R, BONGIOVANNI A, ALBEGGIANAI G. Inhibitory effect of neuraminidase on SP-induced histamine release and TNF alpha in rat mast cells:evidence of a receptor-independent mechanism, 1997(1-5)
[14] KINCY-CAIN T, BOST K L. Substance P-induced IL-12 production by murine macrophages. 1997(50)
[15] SUZUKI H, MIURA S, LIU Y Y. Substance P induces degranulation of mast cells and leukocyte adhesion to venular endothelium. 1995(8). doi:10.1016/0196-9781(95)02050-0  

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 414523 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364