Hoxha Malvina
Department of Chemical-Toxicological and Pharmacological Evaluation of Drugs, Catholic University Our Lady of Good Counsel, Tirana, Albania; Department of Pharmacological and Biomolecular Sciences, Università degli studi di Milano, Milan, Italy.
Adv Med Sci. 2018 Mar;63(1):22-29. doi: 10.1016/j.advms.2017.06.004. Epub 2017 Aug 14.
Rheumatoid arthritis is characterized by the production of eicosanoids, cytokines, adhesion molecules, infiltration of T and B lymphocytes in the synovium and oxygen reduction accompanied by the cartilage degradation. Eicosanoids are responsible for the progressive destruction of cartilage and bone, however neither steroids, nor the non steroidal anti-inflammatory drugs (NSAIDs), cannot slow down cartilage and bone destruction providing only symptomatic improvement. The current rheumatoid arthritis treatment options include mainly the use of disease-modifying anti-rheumatic drugs, the corticosteroids, the NSAIDs and biological agents.
PubMed, Cochrane, and Embase electronic database were used as the main sources for extracting several articles, reviews, original papers in English for further review and analysis on the implication of arachidonic acid metabolites with rheumatoid arthritis and different strategies of targeting arachidonic acid metabolites, different enzymes or receptors for improving the treatment of rheumatoid arthritis patients.
We first focused on the role of individual prostaglandins and leukotrienes, in the inflammatory process of arthritis, concluding with an outline of the current clinical situation of rheumatoid arthritis and novel treatment strategies targeting the arachidonic acid pathway.
Extended research is necessary for the development of these novel compounds targeting the eicosanoid pathway, by increasing the levels of anti-inflammatory eicosanoids (PGD,15dPGJ), by inhibiting the production of pro-inflammatory eicosanoids (PGE, LTB, PGI) involved in rheumatoid arthritis or also by developing dual compounds displaying both the COX-2 inhibitor/TP antagonist activity within a single compound.
类风湿性关节炎的特征在于类二十烷酸、细胞因子、黏附分子的产生，滑膜中T和B淋巴细胞的浸润以及伴随软骨降解的氧减少。类二十烷酸导致软骨和骨骼的进行性破坏，然而，类固醇和非甾体抗炎药（NSAIDs）都无法减缓软骨和骨骼的破坏，仅能提供症状改善。目前类风湿性关节炎的治疗选择主要包括使用改善病情抗风湿药、皮质类固醇、NSAIDs和生物制剂。
使用PubMed、Cochrane和Embase电子数据库作为主要来源，提取多篇英文文章、综述、原始论文，以进一步审查和分析花生四烯酸代谢物与类风湿性关节炎的关系以及针对花生四烯酸代谢物、不同酶或受体的不同策略，以改善类风湿性关节炎患者的治疗。
我们首先关注了个体前列腺素和白三烯在关节炎炎症过程中的作用，最后概述了类风湿性关节炎的当前临床情况以及针对花生四烯酸途径的新治疗策略。
有必要进行进一步研究以开发这些针对类二十烷酸途径的新型化合物，通过提高抗炎类二十烷酸（PGD、15dPGJ）的水平，抑制参与类风湿性关节炎的促炎类二十烷酸（PGE、LTB、PGI）的产生，或者开发在单一化合物中同时具有COX-2抑制剂/TP拮抗剂活性的双重化合物。
