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Phytomedicine

Phytomedicine

IF: 6.7
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Avicularin inhibits ferroptosis and improves cognitive impairments in Alzheimer's disease by modulating the NOX4/Nrf2 axis

Published:31 October 2024 DOI: PMID: 39515096
Zixiang Li , Yingying Lu , Yongqi Zhen , Wenke Jin , Xuelan Ma , Ziyue Yuan , Bo Liu , Xian-Li Zhou , Lan Zhang

Abstract

Background

Alzheimer's disease (AD) is a widespread neurodegenerative disorder for which effective therapies remain elusive, primarily due to the complexity of its underlying pathophysiology. In recent years, natural products have gained attention for their therapeutic potential in AD, owing to their multi-targeted actions and low toxicity profiles. Avicularin (Avi), a flavonoid derived from the peels of Zanthoxylum bungeanum Maxim., has shown promise as an anti-AD agent. However, the specific mechanisms by which Avi mitigates oxidative stress and inhibits ferroptosis in AD models remain insufficiently understood. Further investigation is required to elucidate its therapeutic potential in these pathways.

Purpose

Therefore, this study aims to elucidate the neuroprotective effects of Avi in AD by investigating its impact on the NOX4/Nrf2 signaling pathway, as well as its role in modulating oxidative stress and ferroptosis.

Methods

In this study, an in vitro H2O2-induced oxidative stress model in SH-SY5Y cells was utilized to evaluate the pharmacological efficacy and underlying mechanisms of Avi. Molecular docking, cellular thermal shift assay and bio-layer interferometry assays were conducted to identify potential molecular targets of Avi. Additionally, in vivo models, including scopolamine (SCOP)-induced and APP/PS1 transgenic mice, were employed to assess the cognitive effects of Avi and further explore its associated molecular mechanisms.

Results

Our study demonstrates that Avi effectively attenuates H2O2-induced toxicity in SH-SY5Y cells by reducing apoptosis and enhancing cellular antioxidant defenses. This neuroprotective effect is mediated through the inhibition of NOX4 and the promotion of Nrf2 nuclear translocation. Furthermore, Avi improves cognitive function and mitigates ferroptosis in both SCOP-induced and APP/PS1 transgenic mouse models of AD.

Conclusion

Avi emerges as an effective neuroprotective agent against AD, offering a promising therapeutic approach by targeting the NOX4/Nrf2 signaling axis to alleviate oxidative stress and ferroptosis.

Substances (6)

Materials
Procduct Name CAS Molecular Formula Supplier Price
Donepezil Hydrochloride 120011-70-3 C24H30ClNO3 738 suppliers $5.00-$2406.00
Donepezil Hydrochloride 120011-70-3 C24H30ClNO3 738 suppliers $5.00-$2406.00
Donepezil Hydrochloride 120011-70-3 C24H30ClNO3 738 suppliers $5.00-$2406.00
Donepezil Hydrochloride 120011-70-3 C24H30ClNO3 738 suppliers $5.00-$2406.00
Donepezil hydrochloride 120011-70-3 - Inquiry
Donepezil hydrochloride 120011-70-3 - Inquiry

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