Abstract：
In the context of inflammation and immunity, there are fragmented and observational studies relating to the pharmacological activity of Mangifera indica L. and its main active component, mangiferin. Therefore, we aimed to analyze the potential beneficial effects of this plant extract (MIE, 90 % in mangiferin) in a mouse model of gouty arthritis, to allow the evaluation of cellular immune phenotypes and the biochemical mechanism/s beyond MIE activity. Gouty arthritis was induced by the intra-articular administration of MSU crystals (200 μg 20 µl-1), whereas MIE (0.1-10 mg kg-1) or corresponding vehicle (DMSO/saline 1:3) were orally administrated concomitantly with MSU (time 0), 6 and 12 h after the stimulus. Thereafter, knee joint score and oedema were evaluated in addition to western blot analysis for COX-2/mPGES-1 axis. Moreover, the analysis of pro/anti-inflammatory cyto-chemokines coupled with the phenotyping of the cellular infiltrate was performed. Treatment with MIE revealed a dose-dependent reduction in joint inflammatory scores with maximal inhibition observed at 10 mg kg-1. MIE significantly reduced leukocyte infiltration and activation and the expression of different pro-inflammatory cyto-chemokines in inflamed tissues. Furthermore, biochemical analysis revealed that MIE modulated COX-2/mPGES-1 and mPGDS-1/PPARγ pathways. Flow cytometry analysis also highlighted a prominent modulation of inflammatory monocytes (CD11b+/CD115+/LY6Chi), and Treg cells (CD4+/CD25+/FOXP3+) after MIE treatment. Collectively, the results of this study demonstrate a novel function of MIE to positively affect the local and systemic inflammatory/immunological perturbance in the onset and progression of gouty arthritis.
摘要：
在炎症和免疫的背景下，有零散的和观察性的研究，有关的药理活性的芒果及其主要活性成分，芒果苷.因此,我们旨在分析这种植物提取物的潜在有益作用(MIE，芒果苷中的90％）在痛风性关节炎的小鼠模型中，允许评估细胞免疫表型和MIE活性以外的生化机制。痛风性关节炎由MSU晶体（200μg20μl-1）的关节内给药诱导，而MIE（0.1-10mgkg-1）或相应的媒介物（DMSO/盐水1：3）与MSU同时口服（时间0），刺激后6和12小时。此后,除了对COX-2/mPGES-1轴进行westernblot分析外,还评估了膝关节评分和水肿.此外，对促炎/抗炎细胞趋化因子进行分析,并对细胞浸润物进行表型分析.用MIE治疗显示出关节炎症评分的剂量依赖性降低，在10mgkg-1时观察到最大抑制作用。MIE显着降低了炎症组织中白细胞的浸润和活化以及不同促炎细胞趋化因子的表达。此外，生化分析表明，MIE调节COX-2/mPGES-1和mPGDS-1/PPARγ途径。流式细胞术分析还强调了炎性单核细胞（CD11b/CD115/LY6Chi）的显着调节，MIE处理后的Treg细胞(CD4+/CD25+/FOXP3+)。总的来说，这项研究的结果证明了MIE在痛风性关节炎的发病和进展中积极影响局部和全身炎症/免疫紊乱的新功能.
