【摘要】 目的检测Smad7,Smad2/3总量及活化形式P-Smad2/3在唑酮诱导的实验性结肠炎结肠粘膜中的表达,探讨Smad分子在溃疡性结肠炎发病机制中的可能作用。方法采用免疫印迹及免疫沉淀法检测正常Balb/C小鼠以及唑酮诱导的实验性结肠炎小鼠中肠粘膜组织中Smad7,Smad3/2总量及活化形式P-Smad2/3的表达水平。结果Smad7的表达在实验组明显高于对照组,Smad3和Smad2在实验组与对照组中表达无差别,而P-Smad3实验组明显低于对照组,P-Smad2两组表达并无差别。结论Smad分子异常导致的TGF-β1信号通路障碍影响其抗炎作用的发挥,可能与UC中的慢性炎症产生有关。更多还原

【Abstract】 Objective To observe the expression of Smad7,total Smad3/Smad2 and active Smad3/Smad2（phosphorylated P-Smad3/2） in oxazolone induced colitis of mice and find out the mechanism of the abnormality of Smad on pathogenesis of colitis.Methods The expression level of Smad7,total Smad3/Smad2 and phosphorylated Smad3/Smad2 of intestinal mucosa in oxazolone induced colitis of mice and control were examined by Immunoprecipitation and Western blott.Results The expression of Smad7 in experimental colitis was higher than in normal control,while phosphorylated Smad3 decreased in experimental colitis compared to normal group.There were no difference of total Smad3/Smad2 and P-Smad2 between two groups Conclusion Overpression of Smad7 and reduced phosphorylation of Smad3 is associated with defective TGF-β₁ signaling and compromises the ability of TGF-β₁ to downregulate inflammatory responses in inflamed intestinal mucosa.of ulcerative colitis.更多还原