Myricetin Promotes Migration and Prevents Palmitate-Induced Apoptosis in Cultured Tenocytes Through Ampk-Dependent Pathways

Abstract

Myricetin (Myr), a flavonoid present in vegetables and fruits, has been shown to ameliorate inflammation and oxidative stress in various disease models. However, the effects of Myr on hyperlipidemic tenocytes have not been studied. Herein, we aimed to investigate the effects of Myr on the features of tendinopathy in cultured tenocytes under hyperlipidemic conditions. Reactive oxygen species (ROS) were detected by DCFDA. Hydrogen peroxide (H2O2), malondialdehyde (MDA), and caspase 3 activity were quantified via matched assay kits. Apoptotic cells were detected via TUNEL staining. Proteins investigated in this study were evaluated through Western blotting. Treatment with Myr enhanced tenocyte migration and prevented apoptosis, inflammation and oxidative stress in palmitate-treated tenocytes. Myr treatment increased the phosphorylation of AMPK, and the expression of PGC1 alpha and FGF2. siRNA targeting AMPK abrogated the effects of Myr on palmitate-treated tenocytes. However, FGF2 siRNA reduced the impacts of Myr on only cell migration and ECM signaling. These in vitro results suggest that Myr promotes tenocyte migration and ECM signaling via AMPK/FGF2 signaling and attenuates apoptosis through the AMPK-mediated suppression of inflammation and oxidative stress in hyperlipidemic tenocytes. This study sheds light on therapeutic strategies for treating obesity-related tendinopathy.