【摘要】：目的建立SD幼鼠嗜酸細(xì)胞胃腸炎(EG)模型,探討孟魯司特(MK)對EG幼鼠腸道炎癥的抑制作用。方法 32只3周齡雌性SD幼鼠隨機(jī)分為4組:對照組(M0I0組)、對照干預(yù)組(M0I1組)、模型組(M1I0組)、模型干預(yù)組(M1I1組)。M1I0組和M1I1組幼鼠以卵白蛋白(OVA)為過敏原,AL(OH)3為佐劑,通過腹腔注射致敏聯(lián)合灌胃激發(fā)建立模型。觀察大鼠腸黏膜病理改變、嗜酸性粒細(xì)胞(EOS)密度、肥大細(xì)胞(MC)密度及脫顆粒情況,采用析因設(shè)計(jì)方法分析各因素的效果。結(jié)果 M1I0組幼鼠空腸黏膜炎癥損傷明顯,M1I1組幼鼠空腸黏膜炎癥損傷減輕。M0I0、M0I1、M1I0及M1I1組幼鼠空腸黏膜中EOS密度分別為(8.6±2.2),(8.4±1.9),(26.4±1.8)和(16.4±2.2),MC密度分別為(2.3±0.4),(2.3±0.4),(13.5±0.7)及(4.3±0.6),MC脫顆粒率分別為18.3(16.7,23.3)%,19.1(17.0,22.9)%,76.8(76.0,76.8)%,45.1(43.0,48.6)%;建立OVA-EG模型可顯著增加幼鼠空腸黏膜中EOS密度、MC密度及MC脫顆粒率,使用MK干預(yù)則可顯著降低幼鼠空腸黏膜中EOS密度、MC密度及MC脫顆粒率;激發(fā)后幼鼠空腸黏膜EOS密度、MC密度及MC脫顆粒率均受造模和使用MK干預(yù)兩因素影響,造模與使用MK干預(yù)間存在交互作用。結(jié)論 MK可能通過減少腸黏膜EOS、MC浸潤,降低MC脫顆粒率,從而減輕OVA致敏激發(fā)所致的EG幼鼠腸道炎癥損傷。
[Abstract]:Objective to establish a (EG) model of eosinophilic gastroenteritis in young SD rats and to investigate the inhibitory effect of montelukast (MK) on intestinal inflammation in young EG rats. Methods 32 3-week-old female SD young rats were randomly divided into four groups: control group (M0I0 group), control group (M0I1 group), model group (M1I0 group), model intervention group (M1I1 group). M1I0 group and M1I1 group were treated with ovalbumin (OVA) as allergy AL (OH) 3 as adjuvant. The model was established by intraperitoneal injection of sensitization combined with gastric perfusion. The pathological changes of intestinal mucosa, the density of eosinophilic granulocyte (EOS), the density of mast cell (MC) and the degranulation were observed. 緇撴灉 M1I0緇勫辜榧犵┖鑲犻粡鑶滅値鐥囨崯浼ゆ槑鏄，

本文編號(hào)：2201136