孟鲁司特对嗜酸细胞胃肠炎幼鼠肠道炎症的抑制作用  

The Effect of Montelukast on Inflammatory of the Intestinal Mucosa in Eosinophilic Gastroenteritis Rats

作　　者：张晓燕[1] 吴斌[1] 刘俊红[1] 卢建双[1] 黄欢欢[1] 洪舒婷 

机构地区：[1]福建医科大学附属第一医院儿科,福州350005

出　　处：《福建医科大学学报》2015年第6期360-364,共5页Journal of Fujian Medical University

摘　　要：目的建立SD幼鼠嗜酸细胞胃肠炎(EG)模型,探讨孟鲁司特(MK)对EG幼鼠肠道炎症的抑制作用。方法 32只3周龄雌性SD幼鼠随机分为4组:对照组(M0I0组)、对照干预组(M0I1组)、模型组(M1I0组)、模型干预组(M1I1组)。M1I0组和M1I1组幼鼠以卵白蛋白(OVA)为过敏原,AL(OH)3为佐剂,通过腹腔注射致敏联合灌胃激发建立模型。观察大鼠肠黏膜病理改变、嗜酸性粒细胞(EOS)密度、肥大细胞(MC)密度及脱颗粒情况,采用析因设计方法分析各因素的效果。结果 M1I0组幼鼠空肠黏膜炎症损伤明显,M1I1组幼鼠空肠黏膜炎症损伤减轻。M0I0、M0I1、M1I0及M1I1组幼鼠空肠黏膜中EOS密度分别为(8.6±2.2),(8.4±1.9),(26.4±1.8)和(16.4±2.2),MC密度分别为(2.3±0.4),(2.3±0.4),(13.5±0.7)及(4.3±0.6),MC脱颗粒率分别为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模型可显著增加幼鼠空肠黏膜中EOS密度、MC密度及MC脱颗粒率,使用MK干预则可显著降低幼鼠空肠黏膜中EOS密度、MC密度及MC脱颗粒率;激发后幼鼠空肠黏膜EOS密度、MC密度及MC脱颗粒率均受造模和使用MK干预两因素影响,造模与使用MK干预间存在交互作用。结论 MK可能通过减少肠黏膜EOS、MC浸润,降低MC脱颗粒率,从而减轻OVA致敏激发所致的EG幼鼠肠道炎症损伤。Objective To build eosinophilic gastroenteritis（EG）models with Sprague-Dawley（SD）young rats,to research the inhibiting effect of montelukast（MK）on inflammatory of the intestinal mucosa in EG rats. To provide experimental evidences for the treatment of EG with MK. Methods 32 female SD young rats（three weeks old）were randomly divided into 4groups：the Non-Model Non-Intervene group（M0I0）,Non-Model Intervene group（M0I1）,Model Non-Intervene（M1I0）,and Model Intervene group（M1I1）,8in each group. SD young rats in M1I0,M1I1 groups were sensitized by OVA;and AL（OH）3was used as adjuvant. Through intraperitoneal injection（i.p）combined with gavage sensitization the model was established. The jejunum mucosa pathological changes,the density of EOS,the density of MC,and the percentage of MC degranulation in mice were determined. ANOVA of factorial is used to analyze the effect of each factor. Results The intestinal mucous membrane of jejunum was damaged to some extent in M1I0 group,and the damage in M1I1 group was less. The density of EOS（/HPF）were M0I0（8.6±2.2）,M0I1（8.4±1.9）,M1I0（26.4±1.8）,and M1I1（16.4±2.2）. The density of MC were M0I0（2.3±0.4）,M0I1（2.3±0.4）,M1I0（13.5±0.7）,and M1I1（4.3±0.6）. The percentage of MC degranulation（%）were M0I018.3（16.7,23.3）%,M0I119.1（17.0,22.9）%,M1I0 76.8（76.0,76.8）%,M1I145.1（43.0,48.6）%. OVA-EG model increased the density of EOS,the density of MC and MC degranulation rate,while the MK intervention reduced them significantly in the jejunum mucosa of the pups;By factorial ANOVA,two factors of the model and MK intervention had effect on the density of EOS,MC,and the percentage of MC integrity. There were interactions between the model and MK intervention. Conclusion MK could reduce the OVA sensitized gastrointestinal inflammation of EG effectively.It may be related to reduction in number of EOS,MC,and the percentage of MC degranulation in jejunum.

关 键 词：嗜酸细胞胃肠炎 幼鼠 半胱氨酰白三烯受体拮抗剂 孟鲁司特 

分 类 号：R965[医药卫生—药理学]