Resolvins
Resolvins are autacoids of a specific lipid structure: dihydroxy or trihydroxy metabolites of omega-3 fatty acids, primarily eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) but also the docosapentaenoic acid (DPA), clupanodonic acid. They are members of an expanding class of polyunsaturated fatty acid (PUFA) metabolites termed specialized proresolving mediators (SPMs). Other SPMs include the lipoxins, protectin D1 and its related products, and the maresins. SPMs are locally formed and locally acting cell signaling : they are made by cells and act upon their parent or nearby cells to coordinate functional responses. SPMs possess potent anti-inflammation, tissue protection, and tissue healing activities in diverse animal models and accordingly are proposed to be involved in resolving physiological inflammatory responses. Their failure to form in adequate amounts is also proposed to underlie a broad range of human diseases involving pathological inflammation. Metabolically stable analogs of the SPMs, including the resolvins, are in development and being tested in volunteers with chronic inflammation-related diseases.
Resolvins (Rvs) fall into several sub-classes based on the straight chain PUFA from which they are formed and/or a unique aspect of their structure. The Resolvin Ds (RvDs) are metabolites of the 22-carbon PUFA, DHA (i.e. 4Z,7Z,10Z,13Z,16Z,19Z)-docosahexaenoic acid); the resolvin Es (RvEs) are metabolites of the 20-carbon PUFA, EPA (i.e. 5Z,8Z,11Z,14Z,17Z-5,8,11,14,17-eicosapentaenoic acid); the resolvin Dn-6DPA (RvDsn-6DPA) are metabolites of the DPA isomer, osbond acid (i.e. 4Z,7Z,10Z,13Z,16Z-docosapentaenoic acid); the resolvin Dn-3DPA (RvDn-3DPA) are metabolites of the DPA isomer, clupanodonic acid (i.e. 7Z,10Z,13Z,16Z,19Z)-docosapentaenoic acid); and the resolvin Ts (RvTs) are metabolites of clupanodonic acid that, in contrast to (RvDsn-3DPA (all of which possess a 17S-hydroxyl residue), possess a 17R-hydroxyl residue. Certain isomers of RvDs are termed aspirin-triggered resolvin Ds (AT-RvDs) because their synthesis is initiated by a drug-modified COX2 enzyme to form 17(R)-hydroxyl rather than 17(S)-hydroxyl residue of the ReVEs; however, an as yet unidentified cytochrome P450 enzyme(s) may also forms this 17(R)-hydroxy intermediate and thereby contribute to the production of AT-RvEs. All of the cited resolvins except the RvDsn-6DPAs are metabolites of omega-3 fatty acids; it is proposed that the metabolism of dietary omega-3 fatty acids to these resolvins is an important mechanism by which these diets may ameliorate diverse inflammatory reactions and inflammation-based diseases.
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