Objective: To explore the mechanism of lung injury in the rats suffering from ulcerative colitis (UC )and provide experim entalevidence forclinicaltreatm entby observing the changes of TGF-β1 and SP-A expressions in the lung and the intestines ofthe rats with UC .Methods:Ratmodels with UC were established by colon m u-cous m em brane sensitization and enem a with trinitrobenzene sulfonic acid-50% ethanol, all intervened with herbal com pound prescriptions (the groups oftreatm entbased on the lung and the intestine),herbalm onom ers (m atrine and sodium houttuyfonate) and Western medicine (salazosulfapyridine) by intragastric adm inistration, the contents of TGF-β1 and SP-A in the lung,intestines and the serum were detected with double-antibody sandw ich ELISA method in the beginning and in four weeks after medicated,the expressions of SP-A in the lung and intestines were detected with Western blot method.R esults: The contents of TGF-β1 in the serum were im proved significantly in the beginning and four weeks after medicated; the expressions of TGF-β1 in the lung and intestines of m odel group were increased in the beginning while lowered in the four weeks,and the contents ofTGF-β1 were increased after treating in differentgroups,the rise of TGF-β1 expressions of the lung in the group of treatm entbased on the lung w as the most obvious, the levels of TGF-β1 expressions of the intestines in the group of treatm ent based on the intestines, the groups ofm atrine and sodium houttuyfonate were im proved significantly;the expressions of SP-A in lung were low - ered significantly,the treatm ent couldn't promote its expressions; the expressions of SP-AmRNA and SP-A of the intestines were im proved evidently in the beginning and in four weeks after m edication, the indexes in the others were decreased obviously.Conclusion:After medicated for four weeks,the contents of TGF-β1 in the serum of m odelgroup are raised obviously but decreased in the lung and the intestines, which dem onstrates that it ow ns tissue specificity butnotcaused by the influence of the localto the whole;sodium houttuyfonate ofthe lung m eridian could notably raise the expressions of TGF-β1 in the intestines,itsuggests thatspecial relationship betw een the lung and the intestines,SP-A is existed in the lung and the intestines,related to the mechanism oflung injury of UC rats.%目的：通过观察溃疡性结肠炎（UC）大鼠模型肺、肠组织中转化生长因子-β1（TGF-β1）、肺表面活化蛋白-A（SP-A）表达的改变及中药的干预作用，探讨UC发生肺损伤的机制，并为临床治疗提供实验依据。方法：用结肠黏膜致敏加三硝基苯磺酸-50%乙醇灌肠的方法建立UC大鼠模型，并进行中药复方（从肺论治组和从肠论治组）、中药单体（苦参碱及鱼腥草素钠）及西药对照（柳氮磺胺吡啶）灌胃干预，分别于给药0、4周取材，采用双抗体夹心ELISA法检测肺、肠组织及血清中TGF-β1的含量，采用Western blot法检测肺、肠组织中SP-A蛋白表达水平。结果：0、4周时模型组血清中TGF-β1含量明显升高；0周时，模型组肺、肠组织中抗炎性因子TGF-β1表达增多，4周时表达下降，治疗后各组TGF-β1均有上升趋势，从肺论治组肺组织中TGF-β1表达升高最为明显，而从肠论治组、苦参碱组和鱼腥草素钠组能明显升高肠组织中TGF-β1表达水平；0、4周时，肺组织中SP-A表达明显降低，治疗并不能促进其表达；0、4周时肠组织SP-A mRNA、SP-A表达明显升高，各治疗组均能明显降低其表达。结论：4周时，TGF-β1含量在血清中升高而在肺、肠组织中下降，说明UC的肺部炎症反应不是缘于局部对整体的影响，而是具有组织特异性；归经于肺的鱼腥草素钠能明显升高肠道TGF-β1表达水平，说明肺肠的特殊联系，即肺、肠组织在结构上存在共同的物质基础SP-A，且与UC发生肺损伤的机制相关。
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