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作 者:殷勤[1] 施会敏 曲高婷 张爱青[1] 甘卫华[1] YIN Qin SHI Huimin QU Gaoting ZHANG Aiqing GAN Weihua(Department of Pediatrics ,The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210003, China)
机构地区:[1]南京医科大学第二附属医院儿科,江苏南京210003
出 处:《皖南医学院学报》2016年第4期315-319,共5页Journal of Wannan Medical College
摘 要:目的:应用2,4,6-三硝基苯磺酸(TNBS)诱导的大鼠结肠炎模型研究TGFβ1/smads信号途径在5-氨基水杨酸(5-ASA)抗炎过程中的作用。方法:80只Sprague-Dawley大鼠随机分为对照组(n=20)、造模组(n=20)、TNBS+5-ASA口服组(n=20)、TNBS+5-ASA灌肠组(n=20),采用疾病活动指数、大体评分和组织学评分评价TNBS诱导结肠炎的严重程度,通过RTPCR和Western blot检测TGFβ1、smad2、smad3、smad4和smad7 mRNA和蛋白的表达量。结果:造模组smad2、smad3、smad4mRNA和蛋白表达量明显下降,而smad7的mRNA和蛋白表达量明显升高。5-ASA口服和灌肠均可以上调smad2、smad3和smad4 mRNA和蛋白表达,下调smad7的mRNA和蛋白表达,且5-ASA灌肠均优于5-ASA口服。结论:5-ASA可能通过调节TGFβ1/smads途径的信号转导来改善肠黏膜炎症。Objective: To observe the effect of 5-aminosalicylic acid( 5-ASA) on the TGFβ1 /smads signaling pathway in 2,4,6-trinitrobenzene sulfonic acid( TNBS)-induced colitis in rat models.Methods: Eighty Sprague-Dawley rats were equally randomized into control group,model group,TNBS+5-ASA( oral) and TNBS+5-ASA( enema)( n = 20 for each).The severity of TNBS-induced colitis was assessed using the Disease Activity Index scores,Colon Macroscopic Damage Index and the Histopathological Score.Real-time PCR and western blot were then performed to examine the expression of TGFβ1,smad2,smad3,smad4 and smad7 in each group of rats.Results: Exposure to TNBS+ethanol resulted in a marked decrease in the mRNA and protein expression of smad2,smad3 and smad4,yet increase of smad7.Treatment with TNBS+5-ASA by oral or enema had up-regulated the mRNA and protein expression of smad2,smad3 and smad4,yet down-regulated the expression of smad7.Nevertheless,administration of 5-ASA by enema was superior to oral use in improving the intestinal inflammation and mucosal injury.Conclusion: 5-ASA relieves the intestinal inflammation through the TGFβ1 / smads signaling pathway in animal model of inflammatory bowel disease.
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