N-乙醯葡萄醣胺對小腸發炎模式之黏膜修復及免疫調節作用

目的：本研究目的是探討於發炎恢復期補充不同劑量之 N-乙醯葡萄醣胺對以 dextran sulfate sodium (DSS)誘發之黏膜修復、免疫調節、氧化壓力指標及發炎機制之作用。 材料方法：本實驗以 DSS誘發 C57BL/6J雄性小鼠發炎性腸道疾病(IBD)。將5.5週齡大的 C57BL/6J雄鼠隨機分成2組：Vehicle組(RO水，無纖維AIN-93G飼料)、誘發組(3% DSS水w/w，無纖維AIN-93G飼料)， 5天後將誘發組移除 DSS飲水並分成3組：DSS(0% NAG，AIN-93G飼料)、L-NAG(0.2% NAG，AIN-93G飼料)、及H-NAG(0.8% NAG，AIN-93G飼料)，Vehicle組則攝食AIN-93G飼料。飲食介入7天後以CO2窒息犧牲，收集空腸、迴腸及血漿。分析項目含小腸各部位組織病理狀況、tight juction指標 occludin及ZO1之免疫染色及基因表現、細胞激素 TNF-α及IL-10基因表現、相關發炎路徑中 COX-2、NFκB、JNK、c-JUN之蛋白表現以及血漿中脂質過氧化物濃度。 結果：結果顯示 DSS組的黏膜細胞排列最不完整，H-NAG組的各部位表現皆優於 L-NAG組，且 H-NAG組的修復程度已接近於 Vehicle組。 tight junction免疫染色方面：occludin及 ZO1兩者組間趨勢一致，DSS組顯著低於 Vehicle組，H-NAG組表現最高顯著高於 DSS組。tight junction指標 occludin、ZO1基因表現：occludin及 ZO1結果一致，H-NAG組迴腸部分顯著高於 DSS組。細胞激素 TNF-α、IL-10基因的表現：TNF-α迴腸部分

Objectives：The aim of study was to determine effects of N-acetylglucosamine (NAG) on the mucosa repair, immune function, oxidative stress and inflammatory-related pathway in a dextran sulfate sodium (DSS)-induced inflammatory bowel disease mouse model.Materials and Methods：C57BL/6J mice (age 5.5wk) were randomly divided into vehicle ( RO water) and DSS-induced groups (3% w/v DSS water) for 5 days (induction period) during which mice were fed fiber-free AIN-93 diets. In the following diet period, DSS-induced mice were further assigned to the three experimental groups: DSS (AIN-93G diet, 0% NAG)、L-NAG (0.2% NAG, w/w) and H-NAG (0.8% NAG, w/w) and the vehicle group was fed AIN-93G diet. Mice were sacrificed on day 7 of the diet period and the jejunum, ileum, and plasma were collected. The pathological observation, the immunohistochemistry (IHC) and gene expression of tight junction proteins occluding and ZO1, and the plasma malondialdehyde were determined. In addition, we determined the gene expression of the inflammatory-related factors including tumor necrosis factor-