胃肠病学
胃腸病學
위장병학
Chinese Journal of Gastroenterology
2015年
10期
602-605
,共4页
郭晓榕%刘晓%李洁%吴敏%湛先保
郭曉榕%劉曉%李潔%吳敏%湛先保
곽효용%류효%리길%오민%담선보
急性胰腺炎%替普瑞酮%肠黏膜屏障%紧密连接%Occludin%ZO-1
急性胰腺炎%替普瑞酮%腸黏膜屏障%緊密連接%Occludin%ZO-1
급성이선염%체보서동%장점막병장%긴밀련접%Occludin%ZO-1
Acute Pancreatitis%Teprenone%Intestinal Mucosal Barrier%Tight Junctions%Occludin%ZO-1
背景:肠黏膜屏障功能损害是急性胰腺炎(AP)发生、发展的关键环节,与疾病预后密切相关。目的:探讨黏膜保护剂替普瑞酮对 AP 大鼠模型肠黏膜屏障的保护作用及其可能机制。方法:45只成年雄性 Sprague-Dawley 大鼠随机分为正常对照组(n =5)、AP 模型组(n =20)和替普瑞酮治疗组(n =20)。造模大鼠腹部皮下注射雨蛙素,治疗组造模前后予替普瑞酮灌胃。以 ELISA 法检测血清白细胞介素-1(IL-1)、IL-6、肿瘤坏死因子-α(TNF-α)和淀粉酶水平,分别以光学显微镜和透射电子显微镜观察小肠黏膜组织病理学和超微结构变化,蛋白质印迹法检测紧密连接蛋白 occludin、ZO-1表达。结果:AP 模型组血清 IL-1、IL-6、TNF-α和淀粉酶水平较正常对照组显著升高(P <0.05),小肠黏膜绒毛坏死脱落,上皮细胞间紧密连接明显增宽,occludin、ZO-1蛋白表达下调;替普瑞酮治疗组血清促炎细胞因子和淀粉酶水平较 AP 模型组显著降低(P <0.05),小肠绒毛仍较完整,紧密连接致密,occludin、ZO-1蛋白表达增强。结论:在 AP 大鼠模型中,替普瑞酮可能通过上调紧密连接蛋白表达对肠黏膜屏障发挥保护作用。
揹景:腸黏膜屏障功能損害是急性胰腺炎(AP)髮生、髮展的關鍵環節,與疾病預後密切相關。目的:探討黏膜保護劑替普瑞酮對 AP 大鼠模型腸黏膜屏障的保護作用及其可能機製。方法:45隻成年雄性 Sprague-Dawley 大鼠隨機分為正常對照組(n =5)、AP 模型組(n =20)和替普瑞酮治療組(n =20)。造模大鼠腹部皮下註射雨蛙素,治療組造模前後予替普瑞酮灌胃。以 ELISA 法檢測血清白細胞介素-1(IL-1)、IL-6、腫瘤壞死因子-α(TNF-α)和澱粉酶水平,分彆以光學顯微鏡和透射電子顯微鏡觀察小腸黏膜組織病理學和超微結構變化,蛋白質印跡法檢測緊密連接蛋白 occludin、ZO-1錶達。結果:AP 模型組血清 IL-1、IL-6、TNF-α和澱粉酶水平較正常對照組顯著升高(P <0.05),小腸黏膜絨毛壞死脫落,上皮細胞間緊密連接明顯增寬,occludin、ZO-1蛋白錶達下調;替普瑞酮治療組血清促炎細胞因子和澱粉酶水平較 AP 模型組顯著降低(P <0.05),小腸絨毛仍較完整,緊密連接緻密,occludin、ZO-1蛋白錶達增彊。結論:在 AP 大鼠模型中,替普瑞酮可能通過上調緊密連接蛋白錶達對腸黏膜屏障髮揮保護作用。
배경:장점막병장공능손해시급성이선염(AP)발생、발전적관건배절,여질병예후밀절상관。목적:탐토점막보호제체보서동대 AP 대서모형장점막병장적보호작용급기가능궤제。방법:45지성년웅성 Sprague-Dawley 대서수궤분위정상대조조(n =5)、AP 모형조(n =20)화체보서동치료조(n =20)。조모대서복부피하주사우와소,치료조조모전후여체보서동관위。이 ELISA 법검측혈청백세포개소-1(IL-1)、IL-6、종류배사인자-α(TNF-α)화정분매수평,분별이광학현미경화투사전자현미경관찰소장점막조직병이학화초미결구변화,단백질인적법검측긴밀련접단백 occludin、ZO-1표체。결과:AP 모형조혈청 IL-1、IL-6、TNF-α화정분매수평교정상대조조현저승고(P <0.05),소장점막융모배사탈락,상피세포간긴밀련접명현증관,occludin、ZO-1단백표체하조;체보서동치료조혈청촉염세포인자화정분매수평교 AP 모형조현저강저(P <0.05),소장융모잉교완정,긴밀련접치밀,occludin、ZO-1단백표체증강。결론:재 AP 대서모형중,체보서동가능통과상조긴밀련접단백표체대장점막병장발휘보호작용。
Background:Damage of intestinal mucosal barrier is a key factor in the development and progress of acute pancreatitis(AP),and is closely related with the prognosis of the disease. Aims:To investigate the protective effect and possible mechanism of mucoprotective agent teprenone on intestinal mucosal barrier in rats with experimental AP. Methods:Forty-five adult male Sprague-Dawley rats were randomly divided into normal control group(n = 5),AP model group(n = 20)and teprenone treated group(n = 20). AP model was established by subcutaneous injection of cerulein at abdominal wall. Rats in treated group were intervened with teprenone intragastrically before and after model establishment. ELISA was used for measurement of serum interleukin-1(IL-1),IL-6,tumor necrosis factor-α(TNF-α)and amylase;histopathological and ultrastructural changes of small intestinal mucosa were observed by light microscope and transmission electron microscope;Western blotting was used to detect the expressions of tight junction protein occludin and ZO-1. Results:Serum levels of IL-1,IL-6,TNF-α and amylase in AP model group were significantly higher than those in normal control group(P < 0. 05),accompanied by necrosis and exfoliation of small intestinal villus,widening of intercellular tight junctions and downregulation of occludin and ZO-1 expression. While in teprenone treated group,serum levels of proinflammatory cytokines and amylase were significantly decreased as compared with AP model group(P < 0. 05),the villus of small intestine remained intact,and dense tight junctions were observed. Expressions of occludin and ZO-1 in teprenone treated group were upregulated. Conclusions:Teprenone may protect against intestinal mucosal barrier injury in AP model rats by upregulating tight junction protein expression.