RESUMEN
The main objective of the study was to quantify serum levels of nicotinamide phosphoribosyltransferase (Nampt/pre-B-Cell colony-enhancing factor 1/visfatin) in subjects with a history of retinal vascular occlusions (RVOs), disease conditions characterized by pronounced ischemia, and metabolic energy deficits. A case-control study of 18 subjects with a history of RVO as well as six healthy volunteers is presented. Serum Nampt levels were quantified using a commercially available enzyme-linked immunosorbent assay kit. Serum Nampt levels were 79% lower in patients with a history of RVO compared with that in healthy volunteers (P<0.05). There was no statistically significant difference among the types of RVOs, specifically branch retinal vein occlusions (n=7), central retinal vein occlusions (n=5), hemiretinal vein occlusions (n=3), and central retinal artery occlusions (n=3; P=0.69). Further studies are needed to establish the temporal kinetics of Nampt expression and to determine whether Nampt may represent a novel biomarker to identify at-risk populations, or whether it is a druggable target with the potential to ameliorate the long-term complications associated with the condition, ie, macular edema, macular ischemia, neovascularization, and permanent loss of vision.
RESUMEN
Ischemic stroke is a significant health problem affecting over 6 million people in the United States alone. In addition to surgical and thrombolytic therapeutic strategies for stroke, neuroprotective therapies may offer additional benefit. N-acylethanolamines (NAEs) are signaling lipids whose synthesis is upregulated in response to ischemia, suggesting that they may be neuroprotective. To date only three NAEs, arachidonylethanolamide (NAE 20:4), palmitoylethanolamide (NAE 16:0) and oleoylethanolamide (NAE 18:1) have shown to exert neuroprotective effect in animal models for stroke. Here, we describe neuroprotective effects of the hitherto uncharacterized NAEs, lauroylethanolamide (NAE 12:0) and linoleoylethanolamide (NAE 18:2) in a middle cerebral artery occlusion model of stroke. Pretreatment with NAE 18:2 prior to ischemia/reperfusion (I/R) injury resulted in both significantly reduced cortical infarct volume and improved functional outcome as determined using the neurological deficit score. NAE 12:0 improved neurological deficits without a significant reduction lesion size. Our results suggest that NAEs, as a whole, provide neuroprotection during I/R injury and may have therapeutic benefit when used as complementary treatment with other therapies to improve stroke outcome.