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清肠化湿方对小鼠溃疡性结肠炎模型结肠黏膜上皮细胞Caspase-3、ZO-1的影响 被引量:10

Impacts of Qingchang Huashi Formula on Colonic Epithelial Cell Caspase-3 and ZO-1 in Ulcerative Colitis Models of Mice
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摘要 目的以核因子-κB(nuclear facter-κB,NF-κB)p65反义寡核苷酸(ASODN)及西药柳氮磺胺吡啶(SASP)为对照,观察清肠化湿方对三硝基苯磺酸(TNBS)法诱导小鼠溃疡性结肠炎(UC)模型结肠黏膜天冬氨酸特异酶切的半胱氨酸蛋白酶-3(Caspase-3)、闭锁小带蛋白-1(ZO-1)表达的影响。方法采用TNBS诱导小鼠UC模型,并随机分为清肠化湿方组、SASP组、清肠化湿方+SASP组、ASODN组、模型对照组、空白对照组,治疗7 d后处死小鼠,取小鼠结肠标本,采用HE染色法观察各组小鼠结肠病理形态,并采用Western blot法检测各组小鼠结肠上皮细胞Caspase-3及ZO-1蛋白表达水平。结果模型对照组小鼠Caspase-3蛋白表达明显高于空白对照组(P<0.05);清肠化湿方组Caspase-3蛋白表达低于模型对照组(P<0.05),与空白对照组比较差异无统计学意义(P>0.05)。模型对照组小鼠ZO-1蛋白表达明显低于空白对照组(P<0.05);清肠化湿方组ZO-1蛋白表达高于模型对照组(P<0.05),与空白对照组比较差异无统计学意义(P>0.05)。结论清肠化湿方对UC模型小鼠具有治疗作用,其抑制肠上皮细胞Caspase-3蛋白表达、增强ZO-1的表达,抑制肠黏膜组织细胞凋亡,恢复正常的肠黏膜屏障形态和功能可能是其作用机制的一部分。 Objective To take NF- κB p65 ASODN and the western medicine SASP as the controls to observe the impacts of Qingchang Huashi Formula on the expressions of Caspase- 3 and ZO- 1 in ulcerative colitis( UC) models of mice induced by TNBS methods. Methods TNBS method was adopted to induce UC models,which were randomized into a Qingchang Huashi Formula group( Formula group),a SASP group, Formula + SASP group,ASODN group,a model control group and a blank control group. The mice were sacrificed in 7 days of treatment and the colon samples were collected. HE method was used to observe the pathologic morphology of colons in the experimental mice in each group. Western Blot method was applied to determine the expressions of Caspase- 3 and ZO- 1 in each group. Results Capspase- 3 expression in the model control group was higher apparently than that in the blank control group( P〈0. 05),Capsase- 3 expression in the Formula group was lower than that in the model control group( P〈0. 05),but had no statistical difference as compared with the blank control group( P〈0. 05). ZO- 1 expression in the model control group was lower apparently than that in the blank control group( P〈0. 05),that in the Formula group was higher than that in the model control group( P〉. 05),but had no statistical difference as compared with the blank control group( P〈0. 05). Conclusion Qingchang Huashi Formula had the therapeutic effect on UC models of mice. It suppresses epithelial cell Caspase- 3 expression and intensifies ZO- 1 expression,inhibits intestinal mucosal apoptosis and recovers the normal morphology and function of intestinal mucosal barrier. All of those could be the effect mechanism of the formula.
出处 《世界中西医结合杂志》 2014年第5期473-476,491,共5页 World Journal of Integrated Traditional and Western Medicine
基金 国家自然科学基金资助项目(No.81072778 No.81373606) 江苏省自然科学基金资助项目(No.BK2011078) 江苏省国家中医临床研究基地(脾胃病)开放课题项目(No.JD11002)
关键词 清肠化湿方 CASPASE-3 ZO-1 溃疡性结肠炎 核因子-ΚB QIngchang Huashi Formula Caspase-3 ZO1 Ulcerative Colitis NF-κB
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参考文献16

  • 1江学良,权启镇,陈桂荣,孙自勤,王要军,王玉萍.凋亡调控蛋白在溃疡性结肠炎活检组织中的表达[J].世界华人消化杂志,2000,8(1):107-108. 被引量:8
  • 2毛德文,陈月桥,王丽,武建华.Caspase-8及Caspase-3与细胞凋亡[J].辽宁中医药大学学报,2008,10(10):148-150. 被引量:97
  • 3Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease [ J ]. Nature,2007,448 (7152 ) :427 - 434. 被引量:1
  • 4Dieleman LA, Palmen MJ, Akol H, et al. Chronic experimental colitis induced by dextran sulphate sodium(DSS) is characterized by Thl and Th2 cytokines[ J]. Clin Exp Immunol,1998,114(3) :385 -391. 被引量:1
  • 5Schneeberger EE, Lynch RD. The tight junction: a muhifunctional complex [ J ]. Am J Physiol,2004,286 ( 6 ) : C 1213 - C1228. 被引量:1
  • 6Schulzke JD, Ploeger S, Amasheh M, et al. Epithelial tight junctions in intestinal inflammation [ J]. Ann N Y Acad Sci ,2009,5 (1165 ) : 294 - 300. 被引量:1
  • 7陈少夫,张卫卫,王赫.细胞凋亡与溃疡性结肠[J].世界华人消化杂志,2002,10(4):431-432. 被引量:5
  • 8Raddatz D, Bockemuhl M, Ramadori G. Quantitative measurement of cytokine mRNA in inflammatory bowel disease:relation to clinical and endoscopic activity and outcome [ J ]. Gastroenterol Hepatol, 2005,17 (5) :547 -557. 被引量:1
  • 9Fanning AS, Jameson B J, Jesaitis LA, et al. The tight junction proteon ZO - 1 establishes a link between the transmembrance protein in oc- cluding and the actin eytoskeleton [ J ]. J Biolchem, 1998,273 (45) : 29 745 -29 753. 被引量:1
  • 10Jones SA, Butler RN, Sanderson IR, et al, The effect of specific caspase inhibition on TNF - alpha and butyrate - induced apotosis of intestinal epi the lial cells[ J]. Exp Cell Res ,2004,292 ( 1 ) :29 -39. 被引量:1

二级参考文献56

  • 1溃疡性结肠炎的诊断及疗效标准[J].中华消化杂志,1993,13(6):354-354. 被引量:1064
  • 2刘丽君,彭建新,洪华珠,叶雯,乔媛媛.线粒体在细胞凋亡中的变化与作用[J].细胞生物学杂志,2005,27(2):117-120. 被引量:44
  • 3[2]Tompson CB. Apoptosis in the pathogenesis and treatment of disease. Science 1995;267:1456-1462 被引量:1
  • 4[3]Suzuki A, Sugimura K, Ohtsuka K, Hasegawak, Suzuki K, Ishizuka K, Moehizuki T,Honma T, Narisawa K, Asakura H. Fas/Fas ligand expression and characteristics of primed CD45RO + T cells in the inflamed mucosa of ulcerative colitis. Scand J Gastroenterol 2000;35:1278-1283 被引量:1
  • 5[4]Merritt AJ, Potten CS, Watson AJM, Loh DY, Nakayama K, Nakayama K, Hiekman JA. Differential expression of bcl-2 in intestinal epithelia. J Cell Scienee 1995; 108:2261-2271 被引量:1
  • 6[5]Krajewski S, Krejewska M, Shabaik A., Miyashita T, Wang HG, Reed JC.Immunohistochemical determination of in vivo distribution of Bax, a dominant inhibitor ofBcl-2. Am J Pthol 1994;45:1323-1336 被引量:1
  • 7[6]Arai N, Mitomi H, Ohtani Y, Igarashi M, Kakita A, Okayasu 1. Enhanced epithelial cell turnover associated with p53 accumulation and high P21WAFl/CIP1 expression in ulcerative colitis. Mod Pathol 1999; 12; 604-611 被引量:1
  • 8[8]imura M, Nakamura T, Shinozaki S, Iizuka B, Inoue Y, Suzuki S, Hayashi N. Bax is downregulated in inflamed colonic mucosa of ulcerative colitis. Gut 2000;47:228-235 被引量:1
  • 9[9]Sandoval M, Liu XP, Mannick EE, Clark DA, Miller MJS. Peroxynitrite-induced apoptosis in human intestinal epithelial ,ells is attenuatexl by mesalamine.Gastroenterology 1997; 113:1480-1488 被引量:1
  • 10[10]O' connell J, Bennett MW, Nally K, O' Sullivan GC, Collins JK, Shanahan F.Interferon-gamma sensitizes colonic epithelial cell lines to physiological and therapeutic inducers of colonocyte apoptosis. J Cell Physiol 2000; 185:331-338 被引量:1

共引文献139

同被引文献183

  • 1徐翎翎,洪艳燕,张苏闽,陆琴,丁康.任督灸联合中药保留灌肠治疗脾虚湿蕴型溃疡性结肠炎疗效观察[J].四川中医,2022,40(12):66-69. 被引量:5
  • 2Giovanni C Actis,Floriano Rosina,Rinaldo Pellicano.Inflammatory bowel diseases: Current problems and future tasks[J].World Journal of Gastrointestinal Pharmacology and Therapeutics,2014,5(3):169-174. 被引量:4
  • 3欧阳钦,胡品津,钱家鸣,郑家驹,胡仁伟.对我国炎症性肠病诊断治疗规范的共识意见[J].胃肠病学,2007,12(8):488-495. 被引量:751
  • 4Atreya R, Neurath M F. Involvement of IL-6 in the pathogenesis of inflammatory bowel disease and colon cancer. Clin Rev Allergy lmmunol, 2005, 28(3): 187 - 196. 被引量:1
  • 5Rose-John S, Scheller J, Elson G, et al. Interleukin-6 biology is coordinated by membrane-bound and soluble receptors: role in inflammation and eaneer. JLeukoc Biol, 2006, 80(2):227-236. 被引量:1
  • 6Yamamoto M, Yoshizaki K, Kishimoto T, et al. IL-6 is required for the development of Thl cell-mediated murine colitis. J Immunol, 2000, 164(9):4878-4882. 被引量:1
  • 7Riehards P J, Nowell M A, Horiuchi S, et al. Functional characterization of a soluble gpl30 isoform and its therapeutic capacity in an experimental model of inflammatory arthritis. Arthritis Rheum, 2006, 54(5):1662-1672. 被引量:1
  • 8Hirano T, Akira S, Taga T, et al. Biological and clinical aspects of interleukin 6. Immunol Today, 1990, 11(12):443-449. 被引量:1
  • 9Heinrich P C, Behrmann I, Haan S, et al. Principles of interlenkin (IL)-6-type cytokine signalling and its regulation. Biochem J, 2003, 374(Pt 1):1-20. 被引量:1
  • 10Mitsuyama K, Sata M, Rose-John S. Interleukin-6 trans-sigaling in inflammatory bowel disease. Cytokine Growth Factor Rev, 2006, 17(6):451-461. 被引量:1

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