期刊文献+

溃结康胶囊对TNBS诱导大鼠结肠炎治疗作用的研究 被引量:5

The Effects of Kuijiekang Capsule on Ulcerative Colitis Induced by TNBS in Rats
下载PDF
导出
摘要 目的:探讨溃结康胶囊对TNBS诱导大鼠结肠炎的治疗作用。方法:制备TNBS结肠炎大鼠模型,实验设正常对照组、模型对照组、阳性药物对照组(柳氮磺吡啶, 0. 50g/kg)、溃结康给药组( 0. 64, 0 .32, 0 .16g/kg),采用灌胃方式给药,给药时间从制备模型6d后开始,连续12天。实验结束后观察大鼠结肠粘膜损伤指数(CMDI)、粪便隐血(OB)、髓过氧化物酶(MPO)活性和粘膜病理组织学情况,并检测结肠组织丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH- Px)含量;胸腺、脾脏称重。结果:溃结康可减轻TNBS结肠炎大鼠的CMDI和OB程度,降低MPO水平,可改善结肠粘膜病理损伤;并可明显对抗胸腺萎缩和脾脏肿大;同时溃结康可明显降低MDA含量,增加SOD和GSH- Px水平。结论:溃结康对TNBS诱导的大鼠结肠炎有良好的治疗作用,其机理可能与抗炎、免疫调节和抗氧化损伤有关。 Objective: To evaluate the effects of Kuijiekang Capsule(KJK) on rats colitis induced by TNBS. Methods: Rats with TNBS/ethanol-induced colitis were used and treated with KJK. The experimental animals were divided into 6 groups: control group, model group, SASP group(0.50 g/kg), KJK group(0.64,0.32,0.16 g/kg). The animals were administrated 0.5% carboxymethyl cellulose, SASP and KJK respectively (from the 6 th d after the establishment of ulcerative colitis model to the end of the experiment, 18d totally). At the end of the experiment, the colon mucosal damage index(CMDI), the activity of myelperoxidase(MPO) and the occult blood test(OB) in feces were observed, the mucosa pathohistology was measured and thymus and spleen of rats were weighed respectively. Meanwhile, the content of malondiadehyde(MDA), superoxide dismutase(SOD) and glutathione peroxidase (GSH-Px) of colonic tissue were detected. Results: The remarkable effects of KJK at dosage of 0.64, 0.32 g/kg on TNBS-induced colitis were observed, the extent of CMDI and OB were decrased, MPO activeity of colonic tissue was reduced. The extent of atrophy of thymus gland and intumesce of spleen of rat were ameliorated. Meanwhile, the content of MDA was reduced, and the activities of SOD and GSH-Px were increased. Pathological histology results showed that KJK could alleviate the pathohistological lesion of the colon of rat. Conclusion: Treatment with KJK shows beneficial effects on the mucosal damage of rats colitis induced by TNBS/ethanol. The mechanism of the actions of KJK may relate to anti-inflammatory effect, immunoloregulation and anti-oxidation.
出处 《中药材》 CAS CSCD 北大核心 2005年第4期315-318,共4页 Journal of Chinese Medicinal Materials
  • 相关文献

参考文献9

  • 1郑里,王淑仙,崔德玉,崔艳英.介绍一种简便的炎症性肠疾病的评价方法[J].中国药理学通报,1996,12(5):468-469. 被引量:29
  • 2王皓,欧阳钦,胡仁伟.三硝基苯磺酸结肠炎动物模型的建立[J].胃肠病学,2001,6(1):7-10. 被引量:177
  • 3Kornbluth A, et al. Ulcerative colitis practice guidelines in adults. American college of gastroenterology, practice parameters committee. Am J Gastroenterol, 1997,92(2):204
  • 4Eaden J, et al. Colorectal cancer prevention in ulcerative colitis: a case-control study. Aliment Pharmacol Ther, 2000,14(2):145
  • 5Tsutomu H, et al. Role of Nitric Oxide Synthase Inhibitor in Experimental Colitis Induced by 2,4,6-Trinitrobenzene Sulphonic Acid in Rats. Clinical and Experimental Pharmacology and Physiology, 2001,28(1):9
  • 6Krawisz JE, et al. Quantitative assay for acute intestinal inflammation based on myeloperoxidase activity. Assessment of inflammation in rat and hamster models. Gastroenterology, 1984,87(6):1344
  • 7Little JR, et al. Preparation and characterization of antibodies specific for the 2,4,6-trinitrophenyl group. Biochemistry, 1966,5(11):3385
  • 8Fidler JM. Induction of hapten-specific immunological tolerance and immunity in B lymphocytes. Ⅶ. Correlation between trinitrobenzenesulfonic acid administration, serum trinitrophenyl content, and level of tolerance. Cell Immunol, 1985,94(1):285
  • 9Rachmilewitz D, et al. Inflammatory mediators of experimental colitis in rats. Gastroenterology,1989,97(2):326

二级参考文献7

  • 1Butzner JD, Parmar R, Bell CJ, Dalai V. Butyrateenema therapy stimulates mucosal repair in experimental colitis in the rat. Gut, 1996, 38: 568~573.
  • 2Dieleman LA, Palmen MJ, Akol H, Bloemena E,Pena AS, Meuwissen SG, Van Rees EP. Chronicexperimental colitis induced by dextran sulphatesodium (DSS) is characterized by Th1 and Th2 cy-tokines. Clin Exp Immunol, 1998, 114: 385~391.
  • 3Beagley KW, Black CA, Elson CO. Strain differences in susceptibility to TNBS-induced colitis(abstract). Gastroenterology, 1991, 100: A560.
  • 4Ward M. The pathogenesis of Crohn's disease.Lancet, 1977, 2: 903-905.
  • 5Shorter RG, Huizenga KA, Spencer RJ. A working hypothesis for the etiology and pathogenesisof nonspecific inflammatory bowel disease. Am JDig Dis, 1972, 17: 1024~ 1032.
  • 6Kunin S, Gallily R. Recognition and lysis of altered-self cells by macrophages. I. Modification oftarget cells by 2, 4, 6-trinitrobenzene sulphonicacid. Immunology, 1983, 48: 265~272.
  • 7Grisham MB, Volkmer C, Tso P, Yamada T. Metabolism of trinitrobenzene sulfonic acid by the ratcolon produces reactive oxygen species. Gastroenterology, 1991, 101: 540~547.

共引文献204

同被引文献41

引证文献5

二级引证文献23

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