Coordination of mitochondrial and lysosomal homeostasis mitigates inflammation and muscle atrophy during aging

Our previous studies revealed that echinocystic acid (EA) showed obvious attenuation of atherosclerosis in rabbits fed a high-fat diet. However, the underlying mechanisms remain to be elucidated. Considering importance endothelial progenitor cells (EPCs) atherosclerosis, we hypothesise EPCs may one targets for anti-atherosclerotic potential EA.After vitro cultivation, were exposed 100 μg/mL oxidised low-density lipoprotein (oxLDL) and incubated with or without EA (5 20 μM) 48 h. An additional two groups (oxLDL + μM EA) pre-treated either wortmannin, an inhibitor phosphoinositide 3-kinase (PI3K) pathway, nitro-l-arginine methyl ester (l-NAME), nitric oxide synthase (eNOS)-specific inhibitor. Assessment EPC apoptosis, adhesion, migration, (NO) release was performed using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) staining, cell counting, caspase-3 activity assay, transwell chamber Griess reagent, respectively. The protein expression kinase B (Akt) eNOS detected Western blot.Treatment oxLDL induced significant apoptosis impaired NO production. deleterious effects on attenuated by EA. when wortmannin l-NAME, abrogated. Additionally, significantly down-regulated as well repression Akt phosphorylation.The inhibitory effect Akt/eNOS phosphorylation Taken together, results indicate protects from damage caused via pathway.