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前列腺素E2对阻塞性黄疸大鼠小肠粘膜形态的保护作用 被引量:1

Protection of PGE2 against intestinal mucosa injuries in obstructed jaundice rats
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摘要 目的探讨前列腺素E2(PGE2)对阻塞性黄疸大鼠小肠粘膜的保护作用。方法Wistar大鼠50只,随机分成阻塞性黄疸组(A组)10只、阻塞性黄疸再通组(B组)10只、阻塞性黄疸PGE2干预组(C组)10只、阻塞性黄疸再通加PGE2干预组(D组)10只和假手术组(E组)10只。采用直接结扎法制成阻塞性黄疸大鼠模型。再通组采用导管法再通。结扎后1周给予PGE2,结扎后2周再通,再通手术后1周取标本,观察大鼠小肠粘膜的形态学变化。结果PGE2干预组小肠粘膜损伤评分为(2.21±0.75),手术再通组大鼠小肠损伤评分为(2.05±0.71),均较黄疸组减轻(5.26±0.57,P<0.05)。结论阻塞性黄疸大鼠小肠粘膜明显受损,PGE2及手术再通均可减少其损伤。但两者没有协同作用。 Objective To explore the effect of PGE2 on damage of intestinal mucosa in obstructed jaundice rats. Methods A total of 50 Wistar rats were randomly divided into the obstructive jaundice group (A group, n = 10), the obstructive jaundice recanalization group (B group, n = 10), the obstructive jaundice PGE2 intervention group (C group, n = 10), the obstructive jaundice recanalization and PGE2 intervention group (D group, n = 10) and the sham-operation group (E group, n = 10). Obstructive jaundice models were established by direct ligation. The re-canalization group was used repeffusion catheterization. PGE2 was used one week after ligation, and materials were drawn at 1 week after reperfusion for observation of morphological changes in the rat small intestine. Results Scores in small intestinal injury of the PGE2 intervention group (2.21 ± 0.75) and scores in small intestine injury of the reeanalization group (2.05 ± 0.71 ), were less than the obstructive jaundice group (5.26 ± 0.57, P 〈 0.05). Conclusion Small intestinal mucosa of obstructive jaundice rats was markedly impaired. PGE2 and surgical re-canalization may reduce the injury but they have no synergic effect.
出处 《山东大学学报(医学版)》 CAS 北大核心 2009年第6期12-14,19,共4页 Journal of Shandong University:Health Sciences
关键词 黄疸 阻塞性 前列腺素 小肠 大鼠 WISTAR Obstructed, jaundice Prostaglandin Intestine Rats, Wistar
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  • 1黄志强.黄志强胆道外科学[M].山东科学技术出版社:1999.
  • 2Jho D H, Jho D J, Chejfec G, et al. Primary biliary B-cell lymphoma of the cystic duct causing obstructive jaundice [ J ]. Am Surg, 2007, 73(5) :508-510.
  • 3Paumgartner G, Beuers U. Ursodeoxycholic acid in cholestaticliver disease: Mechanisms of action and therapeuticuse revisited[J]. Hepatology, 2002, 36(3):525-531.
  • 4Yoshidome H, Miyazaki M, Shimizu H, et al. Obstructive jaundice impairs hepatic sinusoidal endothelial cell function and renders liver susceptible to hepatic ischemia/reperfusion [ J]. Hepatology, 2000, 33(1):59-67.
  • 5Chiu C J, Mc Ardle A H, Brown R, et al. Intestinal mucosal lesion in low-flow states. I. A morphological, hemodynamic, and metabolic reappraisal[J]. Arch Surg, 1970, 101(4) :478- 483.
  • 6Inagaki T, Moschetta A, Lee Y K, et al. Regulation of anti- bacterial defense in the small intestine by the nuclear bile acid receptor[J]. Proc Natl Acad Sci USA, 2006, 103(10):3920- 3925.
  • 7Gurleyik E, Coskun O, Usttmdag N, et al. Prostaglandin Elmaintains structttral integrity of intestinal mucosa and prevents bacterial translocation during experimental obstructive jaundice [J]. Invest Surg, 2006, 19(5) :283-289.
  • 8Nagahata Y, Azumi Y, Moritomo H, et al. Impaired response of gastric vessels to prostaglandin E2 in rats with persistent obstructive jaundice[J]. Gastroenterology, 1997, 32(4):521-517.
  • 9Aslan A, Bulbul M, Elpek O, et al. Intestinal prostaglandin E2 expression in rat with obstructive jaundice[ J]. Eur J Pediatr Surg, 2007, 17(6):416-419.
  • 10Gookin J L, Galanko J A, Bhkslager A T, et al. PG-mediated closure of paracellular pathway and not restitution is the primary determinant of barrier recovery in acutely injured porcine ileum[J]. Am J Physiol Gastrointest Liver Physiol, 2003, 285 (5) : G967-G979.

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  • 1夏允,张丽萍.幽门螺杆菌感染对血清中前列腺素E_2水平的影响[J].医师进修杂志,2005,28(12):40-40. 被引量:2
  • 2凌东进,傅华群,李建华.生长抑素对大鼠不同肠段粘膜机械屏障损伤的保护作用[J].江西医学院学报,2006,46(2):5-7. 被引量:1
  • 3Kazuhide Higuchi EU,Toshio Watanabe, Yukiko yoda,et al. Pres- ent status and strategy of NSAIDs-induced small bowel injury[ J]. J Gastroenterol,2009,44(9 ) :879-888.
  • 4Chiu C J, McArdle AH, Brown R, et al. Intestinal mueosal lesion inlowflow states : I. A morphological, hemodynamic, and metabolic reappraisal[ J]. Archives Surgery,1970,101:478.
  • 5Brazeau PVW, Burgus R, Ling N, et al. Hypothalamic polypeptide that inhibits the Secretion of immuoreactive pictuitary growth hormone [ J ] . Science, 1973,179:77-79.
  • 6黄文柱,张亚书,张振书等.非甾体类抗炎药相关性小肠病[M].见:现代小肠病学.北京:军事医学出版社,2003:488.
  • 7KT IB. Intestinal permeability in the pathogenesis of NSAID-ind- uced enteropathy[ J]. J Gastroenterol,2009,44( 19 ) :23-29.
  • 8Satoh HKT. Role of food and enterobacteria in the formation and prevention of small intestinal damage induced by NSAIDs [J]. Front Gastrointest Res Basel Karger,2012 ,30 :52-60.
  • 9Yan aka AJS, Ohmori S. Sulforaphane protects small intestinal mucosa from aspirin/NSAID-induced injury by enhancing host defense systems against oxidative stress and by inhibiting mucosal invasion of anaerobic enterobacteria [ J ] . Curr Pharmaceutic Design,2013,19( 1 ) :157-162.
  • 10Omatsu T,Naito Y, Handa O,et al. Involvement of reactive oxy- gen species in indomethacin-indueed apoptosis of small intestinal epithelial cells [ J ]. J Gastroenterol, 2009,44 ( 19 ) : 30 -34.

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