Mediators of Inflammation / 2020 / Article / Tab 1

Review Article

Resolution of Inflammation in Neurodegenerative Diseases: The Role of Resolvins

Table 1

Studies reporting resolvin protective actions.


E-seriesAlzheimer’s diseaseTreatment with RvE1 and LXA4 reversed the inflammatory process and decreased the neuroinflammation associated with Aβ pathology.[99]
AllergyEnhances T cell and eosinophil clearance; abrogates airway hyperresponsiveness.
RvE1 promoted the clearance of eosinophils and antigen-specific T cells, while reducing the expression of proinflammatory cytokines by dendritic cells and Th17 cells.
[23, 100, 101]
Myocardial ischemia/reperfusion injuryRvE1 reduced infiltration of inflammatory cells and reduced production of inflammatory cytokines, leading to improved recovery of cardiac function.[25]
Chronic low-grade systemic inflammationThe activation of the RvE1-ERV1/ChemR23 axis reduced the inflammatory burden of adipose tissue.[29]
AtherosclerosisIn hyperlipidemic mice, the ERV1/ChemR23 gene deletion led to increased oxidized low-density lipoprotein uptake by macrophages.
Exogenous administration of RvE1 reduced atherosclerosis progression in different animal models.
[32, 3436]

D-seriesAlzheimer’s diseaseDiminished RvD1 production in human Alzheimer’s disease.[102]
Parkinson’s diseaseRvD2 prevents the activation of the TLR4/Nf-κB pathway while RvD1 inhibits Mpp+-induced inflammation in PC12 cells (a cell model of Parkinson’s disease).[103]
AllergyRvD1 enhanced macrophage phagocytosis and clearance of allergens in a murine model of allergic bronchial reaction.[24]
Tissue ischemia/reperfusion injuryProtect from ischemia-reperfusion-induced kidney damage.
The activation of the DRV2/GRP18 axis reduces neutrophil infiltration in a mouse model of hind limb ischemia/reperfusion.
In a mouse model of cerebral ischemia/reperfusion injury, exogenous administration of RvD2 reduced infarction area, inflammatory response, and brain edema.
Chronic low-grade systemic inflammationRvD1 and RvD2 decrease the production of proinflammatory mediators in adipose tissue and reduce monocyte transadipose migration.[30]
AtherosclerosisLevels of RvD1 are reduced in the vulnerable regions of atherosclerotic plaques of fat-fed low-density lipoprotein receptor (Ldlr)-/- mice.
Administration of RvD1 to fat-fed Ldlr-/- mice promotes atherosclerotic plaque stability by reducing lesional oxidative stress and necrosis and improving lesional efferocytosis.

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