6 rezultati
Cardiac fibrosis and inflammation play critical roles in ventricular remodelling after myocardial infarction (MI). Urolithin B (UB), a metabolite of ellagitannin-rich foods, has various biological activities, but its effect on ventricular remodelling after MI has not been determined. The present
Neuroinflammation contributes to neuronal death in cerebral ischemia. Urolithin A (UA), a gut microbial metabolite of ellagic acid, has emerged as a potential anti-inflammatory agent. However, its roles and precise mechanisms in stroke remain unknown. Here we found that UA treatment ameliorated
Ischemia/reperfusion (I/R) induces additional damage to the restoration of blood flow to ischemic myocardium. This study examined the effects of urolithin A (UA) on myocardial injury of ischemia/reperfusion in vivo and vitro and explored its underlying mechanisms. Mice were subjected to myocardial
Mitochondrial autophagy (mitophagy) clears damaged mitochondria and attenuates ischemic neuronal injury. Urolithin A (Uro-A) activates mitophagy in mammal cells and Caenorhabditis elegans. We explored neuroprotection of Uro-A against ischemic neuronal Ischemia/reperfusion (IR) induces additional damage during the restoration of blood flow to ischemic myocardium. Urolithin B (UB) is one of the gut metabolites of ellagitannins, a class of antioxidant polyphenols, which was found to be protective against oxidative stress in multiple organs. However,
OBJECTIVE
Nuts in general and walnuts in particular are in the limelight for the association of their consumption with improved health outcomes. Walnuts have an optimal composition in bioactive nutrients and recent clinical and experimental studies have uncovered a number of beneficial effects of