The Anti-Arthritis Effect of Olive-Derived Maslinic Acid in Mice is Due to its Promotion of Tissue Formation and its Anti-Inflammatory Effects
The Anti-Arthritis Effect of Olive-Derived Maslinic Acid in Mice is Due to its Promotion of Tissue Formation and its Anti-Inflammatory Effects
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橄榄源山楂酸对小鼠的抗关节炎作用是由于其促进组织形成和抗炎作用
DOI：
10.1002/mnfr.201800543
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发表时间：
2018
影响因子：
5.2
通讯作者：
Hino Akihiro
中科院分区：
文献类型：
--
作者：
Shimazu Kyoko;Fukumitsu Satoshi;Ishijima Tomoko;Toyoda Tsudoi;Nakai Yuji;Abe Keiko;Aida Kazuhiko;Okada Shinji;Hino Akihiro
范围以前的研究表明，摄入含有山楂酸（MA）的橄榄果渣提取物，一种三萜，有效地预防和减轻动物和人类的关节炎。在这里，MA的抗关节炎作用的分子机制已被阐明，通过确定基因表达的变化引起的橄榄衍生MA摄入胶原抗体诱导的arthritis（CAIA）mice.Methods and results小鼠分为未处理（CT），CAIA（CA），和CAIA管理MA（CA + MA）组。CA + MA小鼠从第1天开始以200 mg kg-1体重的日剂量喂食MA。然后在第8天诱导CAIA并在第12天评估。与CA组相比，CA + MA组关节炎症状减轻，炎性细胞因子的基因表达减少。滑膜的DNA微阵列分析显示，MA改变了与炎症相关的基因的表达水平，包括糖皮质激素反应，免疫反应，结论MA对关节炎的预防作用可归因于通过Toll样受体信号转导的失活和通过糖皮质激素下调白三烯来促进组织形成以及抑制滑膜中的炎症受体的
ScopeA previous study demonstrated that intake of olive pomace extract containing maslinic acid (MA), a triterpene, effectively prevents and alleviates arthritis in animals and humans. Here, the molecular mechanisms involved in the anti‐arthritis effect of MA have been elucidated by determining gene expression changes induced by olive‐derived MA intake in collagen antibody‐induced arthritis (CAIA) mice.Methods and resultsMice are divided into the untreated (CT), CAIA (CA), and CAIA administered MA (CA + MA) groups. The CA + MA mice are fed MA at a daily dose of 200 mg kg–1of body weight from day 1. CAIA is then induced on day 8 and evaluated on day 12. Arthritis symptoms are alleviated, and the gene expression of inflammatory cytokines is reduced in the CA + MA group compared with the CA group. A DNA microarray analysis of synovial membranes reveals that MA alters the expression levels of genes related to inflammation, including glucocorticoid responses, immune responses, and the extracellular matrix.ConclusionsThe preventive effect of MA on arthritis is attributable to the promotion of tissue formation as well as suppression of inflammation in the synovium via inactivation of Toll‐like receptor signaling and downregulation of leukotrienes through the glucocorticoid receptor.