Abscisic acid ameliorates experimental IBD by downregulating cellular adhesion molecule expression and suppressing immune cell infiltration.
Abscisic acid ameliorates experimental IBD by downregulating cellular adhesion molecule expression and suppressing immune cell infiltration.
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DOI：
10.1016/j.clnu.2010.02.009
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发表时间：
2010-12
期刊：
影响因子：
--
通讯作者：
Bassaganya-Riera J
中科院分区：
文献类型：
--
作者：
Guri AJ;Hontecillas R;Bassaganya-Riera J
脱落酸（阿坝）在改善肥胖、糖尿病和心血管疾病模型中的炎症方面表现出有效性。本研究的目的是确定阿坝是否预防或改善实验性炎症性肠病（IBD）。在用2.5%葡聚糖硫酸钠（DSS）攻击之前，给C57 BL/6 J小鼠喂食含有或不含阿坝（100 mg/kg）的饮食35天。每天评估临床疾病的严重程度。采用组织病理学方法对结肠黏膜病变进行评估，并采用实时定量PCR检测细胞粘附分子和炎症标志物。使用流式细胞术定量血液、脾脏和肠系膜淋巴结（MLN）中的白细胞群。研究了阿坝对脾细胞中细胞毒性T淋巴细胞抗原4（CTLA-4）表达的影响。阿坝显着改善疾病活动，结肠炎和减少结肠白细胞浸润和炎症。这些改善与血管细胞粘附标志物-1（VCAM-1）、E-选择素和粘膜地址素粘附标志物-1（MAdCAM-1）表达的下调有关。阿坝还增加了血液中的CD 4+和CD 8 + T淋巴细胞以及血液中的MLN和调节性T细胞。在体外，阿坝通过PPAR γ依赖性机制增加CTLA-4的表达。我们的结论是，阿坝通过调节T细胞分布和粘附分子的表达来改善肠道炎症。
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). C57BL/6J mice were fed diets with or without ABA (100 mg/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. ABA significantly ameliorated disease activity, colitis and reduced colonic leukocyte infiltration and inflammation. These improvements were associated with down-regulation 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. We conclude that ABA ameliorates gut inflammation by modulating T cell distribution and adhesion molecule expression.
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DOI：
10.1084/jem.20082771
发表时间：
2009-09-28
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Klotz L;Burgdorf S;Dani I;Saijo K;Flossdorf J;Hucke S;Alferink J;Nowak N;Beyer M;Mayer G;Langhans B;Klockgether T;Waisman A;Eberl G;Schultze J;Famulok M;Kolanus W;Glass C;Kurts C;Knolle PA
通讯作者：
Knolle PA
影响因子：
6.3
作者：
Guri, Amir J.;Hontecillas, Raquel;Bassaganya-Riera, Josep
通讯作者：
Bassaganya-Riera, Josep
影响因子：
4.9
作者：
Hanauer, SB
通讯作者：
Hanauer, SB
影响因子：
4.3
作者：
Bassaganya-Riera, Josep;Misyak, Sarah;Hontecillas, Raquel
通讯作者：
Hontecillas, Raquel
影响因子：
6.7
作者：
Axelsson, LG;Landstrom, E;BylundFellenius, AC
通讯作者：
BylundFellenius, AC