Frontiers in nutrition · 2026
Strawberry leaf extract protects dopaminergic neurons by restoring redox and mitochondrial homeostasis.
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Ueda Chiharu, Tokumatsu Tamaki, Sogame Fuka, Chiba Nobuaki, Norikura Toshio, Sasaki Yutaro, Matsui-Yuasa Isao, Kojima-Yuasa Akiko
Аннотация
INTRODUCTION: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons, for which effective disease-modifying strategies remain limited. Mitochondrial dysfunction and oxidative stress are central drivers of PD pathogenesis, highlighting the importance of cellular defense mechanisms targeting these processes.
METHODS: In the present study, we investigated the neuroprotective effects of strawberry leaf extract (SLE), an agricultural by-product rich in polyphenols, using both in vitro and in vivo models of PD.
RESULTS: In SH-SY5Y cells, SLE significantly attenuated rotenone-induced loss of cell viability and suppressed intracellular reactive oxygen species (ROS) production. Mechanistically, SLE promoted nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased the expression of antioxidant genes, including heme oxygenase-1 (HO-1) and p62. Pharmacological inhibition experiments further indicated that activation of AMP-activated protein kinase (AMPK) contributes to SLE-induced Nrf2 activation. In addition to redox regulation, SLE modulated mitochondrial quality control pathways. Time-dependent alterations in mitophagy-related markers, including PINK1, Parkin, LC3, and p62, were observed, accompanied by recovery of mitochondrial membrane potential. These findings suggest that SLE influences mitochondrial homeostasis under oxidative stress conditions. In a rotenone-induced PD mouse model, SLE administration ameliorated motor dysfunction and attenuated the loss of tyrosine hydroxylase-positive dopaminergic neurons in the substantia nigra.
DISCUSSION: Collectively, these results demonstrate that SLE exerts neuroprotective effects through coordinated regulation of the AMPK -Nrf2 signaling axis and mitochondrial quality control pathways. This study provides mechanistic insight into the potential of food-derived bioactive compounds as modulators of neurodegenerative processes and highlights SLE as a promising candidate for PD prevention or intervention.
METHODS: In the present study, we investigated the neuroprotective effects of strawberry leaf extract (SLE), an agricultural by-product rich in polyphenols, using both in vitro and in vivo models of PD.
RESULTS: In SH-SY5Y cells, SLE significantly attenuated rotenone-induced loss of cell viability and suppressed intracellular reactive oxygen species (ROS) production. Mechanistically, SLE promoted nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased the expression of antioxidant genes, including heme oxygenase-1 (HO-1) and p62. Pharmacological inhibition experiments further indicated that activation of AMP-activated protein kinase (AMPK) contributes to SLE-induced Nrf2 activation. In addition to redox regulation, SLE modulated mitochondrial quality control pathways. Time-dependent alterations in mitophagy-related markers, including PINK1, Parkin, LC3, and p62, were observed, accompanied by recovery of mitochondrial membrane potential. These findings suggest that SLE influences mitochondrial homeostasis under oxidative stress conditions. In a rotenone-induced PD mouse model, SLE administration ameliorated motor dysfunction and attenuated the loss of tyrosine hydroxylase-positive dopaminergic neurons in the substantia nigra.
DISCUSSION: Collectively, these results demonstrate that SLE exerts neuroprotective effects through coordinated regulation of the AMPK -Nrf2 signaling axis and mitochondrial quality control pathways. This study provides mechanistic insight into the potential of food-derived bioactive compounds as modulators of neurodegenerative processes and highlights SLE as a promising candidate for PD prevention or intervention.