论文摘要
目的 检测Smad7,Smad3/2总量及其活化形式磷酸化的P-Smad3/2在噁唑酮诱导的实验性结肠炎中的表达,探讨Smad分子异常在结肠炎发病机制中可能的作用;并通过检测UC患者中Smad7分子与IκBα之间的表达关系,进一步探讨I-Smad增高对人类溃疡性结肠炎患者肠粘膜免疫紊乱的影响。 材料与方法 1.建立噁唑酮诱导的实验性结肠炎模型:第0天和第1天,雌性Balb/C小鼠腹部皮肤剃毛（2×2cm）,皮肤涂抹200ul 3%噁唑酮（溶解在100%的乙醇中）,第7天灌肠给予150ul 1%噁唑酮（溶解在50%的乙醇中）,灌肠后2～3天将其处死,取结肠进行炎症程度评价,并将造模成功的小鼠分为实验组（8只）,取病变明显处的结肠组织,同时取未经任何处理的对照组小鼠（8只）的结肠组织进行免疫印迹法定量检测结肠粘膜组织中的Smad7,Smad3/2和P-Smad3/2。 2.收集UC患者及正常结肠粘膜标本,采用免疫组化检测UC及正常结肠粘膜组织中Smad7和IκBα的表达情况,并进行半定量图像分析。评价Smad7和IκBα的相关性。
论文目录
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