Abstract
Lipoxins (LXs) are generated from arachidonic acid and are involved in the resolution of inflammation and confer protection in a variety of pathological processes. In the nervous system, LXs exert an array of protective effects against neurological diseases, including ischemic or hemorrhagic stroke, neonatal hypoxia-ischemia encephalopathy, brain and spinal cord injury, Alzheimer’s disease, multiple sclerosis, and neuropathic pain. Lipoxin administration is a potential therapeutic strategy in neurological diseases due to its notable efficiency and unique superiority regarding safety. Here, we provide an overview of LXs in terms of their synthesis, signaling pathways and neuroprotective evidence. Overall, we believe that, along with advances in lipoxin-related drug design, LXs will bring brighter prospects for neuroprotection.
Highlights
Resolution is a crucial stage of the inflammatory response, which is necessary to limit excessive tissue injury, minimize the development of chronic inflammation and re-establish homeostasis
Endogenous LXs can be categorized into two types: native LXs composed of lipoxin A4 (5S,6R,15S-trihydroxy-7,9,13-trans-11cis-eicosatetraenoic acid, LXA4) and lipoxin B4 (5S,14R,15S-trihydroxy-6,10,12-trans-8-cis eicosatetraenoic acid, LXB4) and aspirin-triggered lipoxins (ATLs), including aspirin-triggered lipoxin A4 (15-epi-LXA4, ATLA4) and aspirin-triggered lipoxin B4 (15-epi-LXB4, ATLB4)
They demonstrated that LXA4 could inhibit 5-LOX translocation and leukotriene biosynthesis both in vivo and in vitro, which are partly mediated by formyl peptide receptor 2 (FPR2)/ALX and through an extracellular signal-regulated kinase (ERK) signal transduction pathway (Wu et al, 2012a)
Summary
Resolution is a crucial stage of the inflammatory response, which is necessary to limit excessive tissue injury, minimize the development of chronic inflammation and re-establish homeostasis. In the past few decades, the actions of LXs in inflammation have been gradually determined They can decrease the production of proinflammatory mediators, including interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-α; facilitate the release of anti-inflammatory cytokines such as transforming growth factor-β1, IL-10 and prostaglandin E2 (PGE2); and promote the resolution of inflammation. They are found to inhibit neutrophil chemotaxis and infiltration, promote the phagocytic clearance of apoptotic cells by macrophages, and stimulate the accumulation of a nonphlogistic type of monocytes/macrophages (Lawrence et al, 2002; Maderna and Godson, 2009). We aimed to summarize the current knowledge about the many effects that LXs have on the nervous system and to discuss their roles in different CNS cell types, as well as their therapeutic potential for neurological diseases
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