Attenuation by dietary taurine of dextran sulfate sodium-induced colitis in mice and of THP-1-induced damage to intestinal Caco-2 cell monolayers
Attenuation by dietary taurine of dextran sulfate sodium-induced colitis in mice and of THP-1-induced damage to intestinal Caco-2 cell monolayers
复制标题
DOI：
10.1007/s00726-007-0562-8
复制
发表时间：
2008-06-01
期刊：
影响因子：
3.5
通讯作者：
Shimizu, M.
中科院分区：
文献类型：
--
作者：
Zhao, Z.;Satsu, H.;Shimizu, M.
研究了牛磺酸对葡聚糖硫酸钠（DSS）诱导的小鼠实验性结肠炎的影响。给C57 BL/6雌性小鼠饮用含3%DSS的饮用水5 d，以诱导急性结肠炎。在DSS治疗前5 d和治疗期间，在饮用水中加入2%的牛磺酸，以研究其预防效果。补充牛磺酸显著减弱了DSS诱导的体重下降、腹泻严重程度、结肠缩短和结肠组织髓过氧化物酶活性增加。牛磺酸还显著抑制促炎趋化因子巨噬细胞炎性蛋白2（MIP-2）的表达增加，但不抑制白细胞介素（IL）-1 β或肿瘤坏死因子（TNF）-α mRNA的表达增加。此外，牛磺酸显着保护肠Caco-2细胞单层的巨噬细胞样THP-1细胞在体外共培养系统的损害。这些结果表明，牛磺酸预防DSS诱导的结肠炎部分与（1）其对肠上皮细胞分泌MIP-2和中性粒细胞等炎性细胞浸润的抑制作用和（2）其对DSS直接毒性和炎性细胞诱导的损伤的上皮屏障的细胞保护作用有关。
The effects of dietary taurine on the experimental colitis induced by dextran sulfate sodium (DSS) in mice were evaluated. C57BL/6 female mice were given 3% DSS in drinking water for 5 d to induce acute colitis. Taurine at 2% was added to the drinking water 5 d before and during the DSS-treatment to investigate its preventive effect. Taurine supplementation significantly attenuated the weight decrease, diarrhea severity, colon shortening, and the increase in the colonic tissue myeloperoxidase activity induced by DSS. Taurine also significantly inhibited the increase in the expression of a pro-inflammatory chemokine, macrophage inflammatory protein 2 (MIP-2), but not of interleukin (IL)-1 beta or tumor necrosis factor (TNF)-alpha mRNA. Furthermore, taurine significantly protected the intestinal Caco-2 cell monolayers from the damage by macrophage-like THP-1 cells in an in vitro coculture system. These results suggest that taurine prevented DSS-induced colitis partly in association with (1) its inhibitory effects on the secretion of MIP-2 from the intestinal epithelial cells and on the infiltration of such inflammatory cells as neutrophils and (2) its cytoprotective functions on the epithelial barrier from the direct toxicity of DSS and from the inflammatory cell-induced injury.