Thus, it is imperative to explore more effective treatment strategies to improve the prognosis of neonatal hypoxic-ischemic (HI) brain damage. The treatment effects of hypothermia on moderate or severe patients are very limited, and even have many adverse reactions ( Michniewicz et al., 2022). Despite the application of hypothermia as the reliable standard therapy for neonatal HIE, the treatment time window of hypothermia is very narrow ( Sahuquillo and Vilalta, 2007 Goswami et al., 2020). HIE is not a single occurrence, but is an ongoing process that leads to neuronal death within hours to days after the initial injury ( Jaworska et al., 2017). The nearly half of HIE patients die in the neonatal period, and surviving infants have a high risk of neurological sequelae, which can cause global public health burden ( Rocha-Ferreira and Hristova, 2015). Perinatal asphyxia-induced hypoxic-ischemic encephalopathy (HIE) is one of the important causes of neonatal death and nervous system dysfunction ( Sun et al., 2017). In addition, the NRF2 inhibitor M元85 could significantly reverse the effects of myricetin.Ĭonclusion: This study found that myricetin might alleviate oxidative stress and apoptosis through NRF2 signaling pathway to exert the protective role for HI injury, which suggested that myricetin might be a promising therapeutic agent for HIE. Results: Our results showed that myricetin intervention could significantly reduce brain infarction volume, glia activation, apoptosis, and oxidative stress marker levels through activating NRF2 (Nuclear factor-E2-related factor 2) and increase the expressions of NRF2 downstream proteins NQO-1 and HO-1. Methods: In this study, we established the neonatal rats hypoxic-ischemic (HI) brain damage model in vivo and CoCl 2 induced PC1 2 cell model in vitro to explore the neuroprotective effects of myricetin on HI injury, and illuminate the potential mechanism. However, the role and underlying molecular mechanism of myricetin on HIE remain unclear. Myricetin, a naturally extracted flavonol compound, exerts remarkable effects against oxidative stress, apoptosis, and inflammation. Both oxidative stress and apoptosis play critical roles in the pathological development of HIE. Introduction: Hypoxic-ischemic encephalopathy (HIE) is a crucial cause of neonatal death and neurological sequelae, but currently there is no effective therapy drug for HIE.
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