ArticleNeurochemical research2024
Atractylenolide-I Attenuates MPTP/MPP
Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Molecular regulation of PGC-1α: from protein-protein interactions and post-translational modifications to pharmacological modulation.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Targeted metabolomics to assess positive effects of empagliflozin in a Parkinson's disease model: focused on the kynurenine pathway and oxidative stress.Scientific reports · 2026Article
- Dual-Pathway Defense: Ultramicro-Pulverised Powder ofFood science & nutrition · 2026Article
- Review
- FGF21 confers neuroprotection in Parkinson's disease by activating the FGFR1-sirt1 pathway.Cellular & molecular biology letters · 2025Article
- Celastrol Activates SIRT1/PGC-1α/Nrf2 Axis to Inhibit Oxidative Damage for Subconjunctival Fibrosis Alleviation.Investigative ophthalmology & visual science · 2025Article
- Atractylenolide I Inhibits Nicotine-Induced Macrophage Pyroptosis and Alleviates Atherogenesis by Suppressing the TLR4/ROS/TXNIP/NLRP3 Pathway.Metabolites · 2025Article
- Nuclear receptor coactive 4-mediated ferritinophagy: a key role of heavy metals toxicity.Archives of toxicology · 2025Review
- Atractylenolide I prevents acute liver failure in mouse by regulating M1 macrophage polarization.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is typically marked by motor dysfunction accompanied by loss of dopaminergic (DA) neurons and aggravated oxidative stress in the substantia nigra pars compacta (SNpc). Atractylenolide-I (ATR-I) is a potent antioxidant sesquiterpene with neuroprotective properties. However, whether ATR-I plays a neuroprotective role against oxidative stress in PD remains unclear. The objective of this study was to explore the mechanism of antioxidant action of ATR-I in PD models both in vivo and in vitro. Here, we show that ATR-I alleviated motor deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mice. Moreover, ATR-I treatment effectively reduced DA neuron loss and increased tyrosine hydroxylase expression in the SNpc of MPTP-induced mice. Additionally, ATR-I inhibited oxidative stress (as manifested by elevated superoxide dismutase and glutathione peroxidase activities, and reduced malondialdehyde content) in MPTP-induced mice and attenuated reactive oxygen species levels in 1-methyl-4-phenylpyridinum (MPP
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.