中文摘要：

目的探讨转录信号传导子与激活子3（STAT3）信号传导通路在大鼠急性结肠炎应激反应中的作用。方法自大鼠肛门注入6％醋酸建立急性结肠炎应激模型；应用5级法进行结肠炎症组织学分期；采用免疫印迹法（Western blot）检测脊髓中STAT3蛋白表达水平。结果结肠内灌注6％醋酸可产生明显局部炎症反应，程度随时间进行性加重，16～24h达高峰（16h分级3．5±0．63，24h分级3．0±1．27）；急性结肠炎后L5-S1脊髓内STAT3表达明显上调，3h达高峰，明显高于sham组（P〈0．05）；吗啡治疗对L5-S1、C2-4脊髓内STAT3的表达无明显影响（P〉0．05）。结论大鼠急性结肠炎时，STAT3的上调与炎症应激有关，STAT通路可能并未直接参与介导结肠炎症性疼痛。

英文摘要：

Objective To investigate the role of STAT3 signal pathway in the stress of acute colitis models. Methods The models of acute colitis were induced by 6 % intracolonic acetic acid in rats. The extent of colonic inflammation was assessed by histological examination and scored to 0-4 grade. The spinal STAT3 levels were measured by Western blot at L5-S1 and （22-4 levels. Results There were obvious regional inflammatory responses after intracolonic acetic acid in rats. The extent of inflammation was gradually aggravated with the time prolonged. The histological grade in experimental group was significantly higher than that of naive and sham groups after 3 h and 6 h respectively （P 〈 0.05） and higher than that of naive and sham groups during 16 h to 24 h respectively （P 〈 0.01 ）. The expression of spinal STAT3 at L5-S1 level was significantly increased. The expression in experimental group was significantly higher than in sham group at the peak of 3 h （P〈 0.05）. There were no significant differences in STAT3 levels between morphine-treated group and control group （P 〉0.05）. Conclusion In acute colitis models, the increase of STAT3 may be related with inflammatory stress. However, STAT signal path- way may not mediate the inflammatory pain.