小鼠葡聚糖硫酸钠结肠炎模型结肠黏膜中5-羟色胺及其转运蛋白的变化和意义

背景：小鼠葡聚糖硫酸钠（DSS）结肠炎模型的组织学特点与人类溃疡性结肠炎（UC）类似。5-羟色胺（5-HT）是胃肠道重要的神经递质，其在UC中的变化和意义鲜见报道。目的：测定小鼠DSS结肠炎模型结肠黏膜中5-HT和5-HT转运蛋白（SERT）的变化，探讨UC是否与5-HT信号转导失衡有关。方法：36只C57BL／6小鼠随机分为急、慢性DSS结肠炎组和正常对照组，以免疫组化方法检测5-HT和SERT的表达，以免疫荧光技术检测SERT的免疫反应性。结果：与正常对照组相比，急、慢性DSS结肠炎组远段和近段结肠黏膜5-HT平均灰度值显著降低（含量增加，P〈0．05），远段结肠黏膜SERT平均灰度值显著增高（含量降低，P〈0．05）。正常对照组、慢性和急性DSS结肠炎组结肠黏膜依次发出耀眼、明亮和微弱的黄绿色荧光，提示DSS结肠炎组SERT免疫反应性减弱。结论：DSS诱导的结肠炎促使小鼠结肠黏膜中5-HT含量和SERT的表达发生变化，5-HT和SERT可能参与了UC发生的病理生理机制。

Changes and Significance of 5-Hydroxytryptamine and Serotonin Transporter in Colonic Mucosa of Mice Colitis Model Induced by Dextran Suffate Sodium

Background: Dextran sulfate sodium (DSS)-induced mice colitis mimics human ulcerative colitis (UC) in histological features. 5-hydroxytryptamine (5-HT) is an important gastrointestinal neurotransmitter, however, few studies have focused on its changes and significance in UC. Aims: To investigate the changes of 5-HT and serotonin transporter (SERT) in the colonic mucosa of DSS-induced mice colitis model, and to explore whether imbalance of 5-HT signaling is involved in the pathogenesis of UC. Methods: Thirty-six C57BL/6 mice were randomly divided into acute, chronic DSS-colitis groups and normal control group. Immunohistochemistry was used to detect the expression of 5-HT and SERT, and the immunoreactivity of SERT was assessed by immunofluorescence assay. Results: Compared with the normal control group, the average gray scale of 5-HT in the distal and proximal colonic mucosa of the acute and chronic DSS-colitis groups decreased significantly (P<0.05), whereas the average gray scale of SERT in the distal colonic mucosa increased markedly (P<0.05). Dazzling, bright and faint flavo-green fluorescence was observed in the colonic mucosa of normal control group, chronic and acute DSS-colitis groups, respectively, which demonstrated that the SERT immunoreactivity of the DSS-colitis groups was attenuated. Conclusions: The changes of 5-HT and SERT in mice colonic mucosa are the results of DSS-induced colitis. 5-HT and SERT may be involved in the pathophysiological mechanisms of UC.