Abstract
目的：探讨姜黄素通过信号传导与转录激活因子3（signal transducer and activator of transcription 3,STAT3）通路对小鼠溃疡性结肠炎（ulcerative colitis,UC）模型的作用,以及姜黄素对环氧合酶-2（cyclooxygenase-2,COX-2）、过氧化物酶体增殖物激活受体-g（peroxisome proliferator-activated receptor-g,PPAR-γ）的影响.方法：将♀BALB/c小鼠60只,随机分为6组,每组10只.A组：正常对照组;B组：模型组;C组：地塞米松组[1.5 mg/（kg·d）];L组：姜黄素低剂量组[25 mg/（kg·d）];M组：姜黄素中剂量组[50 mg/（kg·d）];H组：姜黄素高剂量组[100 mg/（kg·d）].小鼠UC模型采用葡聚糖硫酸钠诱导,观察小鼠疾病活动指数（disease activity index,DAI）评分,HE染色观察结肠组织学改变以及免疫组织化学测PPAR-γ、STAT3,ELISA测COX-2的表达,Western blot测p-STAT3的表达,逆转录-聚合酶链反应（reverse transcriptionpolymerase chain reaction,RT-PCR）测STAT3mR NA的表达.结果：（1）B组小鼠症状、组织学都符合UC标准,DAI评分和组织学评分均高于A组,C组、L组、M组、H组DAI评分和组织学评分较B组都有不同程度的下降;（2）免疫组织化学显示：B组小鼠结肠PPAR-γ低于A组（23.15±2.33 vs 42.07±3.82,P〈0.01）;B组小鼠结肠STAT3比A组、C组、L组、M组、H组高（66.36±6.08 v s 28.25±2.84,29.84±3.32,45.26±5.42,29.02±3.28,21.22±3.30,P〈0.01）;（3）ELISA显示与B组相比,C组、L组、M组、H组C O X-2含量较B组低（P〈0.01）;（4）Western blot检测显示B组p-STAT3蛋白水平相比A组明显上升,C组、L组、M组、H组水平较B组降低（P〈0.05）;（5）RT-P C R显示结肠组织S TAT3 m R N A的表达：B组STAT3 m RNA表达水平相比A组明显上升,C、L、M、H组水平较B组降低（P〈0.05）.结论：（1）STAT3、PPAR-γ可能参与了溃疡性结肠炎的发病;（2）姜黄素治疗小鼠UC模型的机制可能通过提高PPAR-γ的含量,抑制STAT3信号通路,减少COX-
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