Myricetin improves apoptosis after ischemic stroke via inhibiting MAPK-ERK pathway.

Abstract

Neuronal apoptosis is the main cause for the disabilities and deaths of patients suffered with stroke. Neuroprotectants are clinically used to reduce neuronal apoptosis in ischemic stroke. However, the current neuroprotectants have multiple limitations. Myricetin is beneficial for multiple neurodegenerative diseases, but the role of myricetin as a neuroprotective agent in ischemic stroke is still not fully understood. Middle cerebral artery occlusion, Terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and Western blots were used to explore the anti-apoptotic effects of myricetin in vivo. Flow cytometry, Western blots and Ca2+ staining were used to study the neuroprotective effects of myricetin in vitro. In this study, we first demonstrated that myricetin reduced neuronal apoptosis after ischemia in vivo and in vitro. And, among the factors of apoptosis after ischemic stroke, excitotoxicity, oxidative stress and inflammation-induced apoptosis can be alleviated by myricetin. Moreover, we further demonstrated that myricetin was able to improve neuronal intrinsic apoptosis by inhibiting the phosphorylation of extracellular signal-regulated kinase in the oxygen and glucose deprivation in vitro. Summarily, our results support myricetin as a novel neuroprotectant for the prevention or treatment of ischemic stroke via MAPK-ERK signaling pathway.