脱落酸通过下调细胞黏附分子表达和抑制免疫细胞浸润来改善实验性 IBD。
Abscisic acid ameliorates experimental IBD by downregulating cellular adhesion molecule expression and suppressing immune cell infiltration.
机构信息
Laboratory of Nutritional Immunology & Molecular Nutrition, Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.
出版信息
Clin Nutr. 2010 Dec;29(6):824-31. doi: 10.1016/j.clnu.2010.02.009. Epub 2010 Mar 16.
BACKGROUND & AIMS: Abscisic acid (ABA) has shown effectiveness in ameliorating inflammation in obesity, diabetes and cardiovascular disease models. The objective of this study was to determine whether ABA prevents or ameliorates experimental inflammatory bowel disease (IBD).
METHODS
C57BL/6J mice were fed diets with or without ABA (100mg/kg) for 35 days prior to challenge with 2.5% dextran sodium sulfate (DSS). The severity of clinical disease was assessed daily. Colonic mucosal lesions were evaluated by histopathology, and cellular adhesion molecular and inflammatory markers were assayed by real-time quantitative PCR. Flow cytometry was used to quantify leukocyte populations in the blood, spleen, and mesenteric lymph nodes (MLN). The effect of ABA on cytotoxic T-lymphocyte antigen 4 (CTLA-4) expression in splenocytes was also investigated.
RESULTS
ABA significantly ameliorated disease activity, colitis and reduced colonic leukocyte infiltration and inflammation. These improvements were associated with downregulation in vascular cell adhesion marker-1 (VCAM-1), E-selectin, and mucosal addressin adhesion marker-1 (MAdCAM-1) expression. ABA also increased CD4(+) and CD8(+) T-lymphocytes in blood and MLN and regulatory T cells in blood. In vitro, ABA increased CTLA-4 expression through a PPAR γ-dependent mechanism.
CONCLUSIONS
We conclude that ABA ameliorates gut inflammation by modulating T cell distribution and adhesion molecule expression.
背景与目的
脱落酸（ABA）已被证明在改善肥胖、糖尿病和心血管疾病模型中的炎症方面具有有效性。本研究的目的是确定 ABA 是否可预防或改善实验性炎症性肠病（IBD）。
方法
C57BL/6J 小鼠在接受 2.5%葡聚糖硫酸钠（DSS）挑战前，用含或不含 ABA（100mg/kg）的饮食喂养 35 天。每日评估临床疾病的严重程度。通过组织病理学评估结肠黏膜损伤，通过实时定量 PCR 测定细胞黏附分子和炎症标志物。使用流式细胞术定量分析血液、脾脏和肠系膜淋巴结（MLN）中的白细胞群。还研究了 ABA 对脾细胞细胞毒性 T 淋巴细胞相关抗原 4（CTLA-4）表达的影响。
结果
ABA 可显著改善疾病活动度、结肠炎并减少结肠白细胞浸润和炎症。这些改善与血管细胞黏附分子-1（VCAM-1）、E-选择素和黏膜地址素细胞黏附分子-1（MAdCAM-1）表达下调相关。ABA 还增加了血液和 MLN 中的 CD4(+)和 CD8(+)T 淋巴细胞以及血液中的调节性 T 细胞。体外，ABA 通过 PPARγ 依赖性机制增加 CTLA-4 表达。
结论
我们得出结论，ABA 通过调节 T 细胞分布和黏附分子表达来改善肠道炎症。
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