ORIGINAL RESEARCH article
Front. Cell Dev. Biol.
Sec. Signaling
This article is part of the Research TopicAntioxidants in Mitigating Oxidative Stress-Induced DamageView all 6 articles
Reduced levels of nitrated α-synuclein in rotenone-induced cellular models of Parkinson's disease after harpagoside treatment
Provisionally accepted
- 1Shaoxing People's Hospital, Shaoxing, China
- 2Shaoxing Second Hospital, Shaoxing, China
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Introduction: Parkinson's disease (PD) ranks as the second most common neurodegenerative disorders following Alzheimer's disease, involving roughly 1% of individuals aged over 60 years. This disorder manifests in affected neural tissues. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) and are implicated in Lewy bodies exhibit nitration and S-nitrosylation. α-synuclein misfolding and neurotoxic effects are applied to induce cellular damage in Neuro-2A cells and BV-2 microglial cells. Harpagoside, acetylharpagide, and harpagide, constituents from Scrophularia ningpoensis Hemsl, were investigated for their neuroprotective potential, serving as reference compounds. Cell viability was assessed using the CCK-8 assay, nitric oxide levels were measured via the nitrososorbent assay (ELISA), and nitrated α-synuclein expression was demonstrated through immunocytochemistry. Results: Our studies revealed substantial cytoprotective effects on rotenone-treated N2A cells. Furthermore, detailed pathway analysis indicated that harpagoside showed its ability to suppress NO generation and inhibit α-synuclein nitration involved in the nuclear factor-κB (NF-κB)/ NOS/NO signaling cascade. In conclusion: Detailed investigation focused on harpagoside's protective actions on α-synuclein nitration involved in the signaling cascade.
Keywords: Iridoid, Harpagoside, Parkinson's disease (PD), α-Synuclein, Nitric Oxide, Nitration, Rotenone
Received: 07 May 2025; Accepted: 23 Oct 2025.
Copyright: © 2025 Lang and Xiong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Zhongkui Xiong, xiongzk@yeah.net
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