ArticlePeerJ2022
Icaritin attenuates 6-OHDA-induced MN9D cell damage by inhibiting oxidative stress.
Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Icaritin ameliorates MPTP-induced Parkinson's disease model by targeting the NLRP3 inflammasome pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Role and Molecular Mechanism of Icaritin in the Treatment of Alzheimer's Disease.Current medicinal chemistry · 2026Review
- Neuroprotective Effects of Rhamnosyl Icariside II in 6-OHDA-Treated PC12 Cells and Zebrafish.Molecular neurobiology · 2025Article
- Icaritin alleviates motor impairment and osteoporosis in Parkinson's disease mice via the ER-PI3K/Akt pathway.Scientific reports · 2025Article
- Therapeutic Effects and Mechanisms of Icaritin in Parkinson's Disease.Current pharmaceutical design · 2025Review
- Cellular Models of Alpha-Synuclein Aggregation: What Have We Learned and Implications for Future Study.Biomedicines · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: We assessed whether ICT can alleviate 6-OHDA-induced cell damage Methods: MN9D cells were treated with 6-OHDA, to study the mechanism underlying the neuroprotective effect of ICT. MN9D cell damage was assessed by the CCK-8 assay, flow cytometry was performed to measure the content of reactive oxygen species (ROS) in cells, a superoxide dismutase (SOD) kit was used to evaluate SOD activity, and Western blotting was used to measure the expression of α-synuclein (α-Syn), Tyrosine hydroxylase (TH), nuclear factor erythroid-2 related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Results: ICT reduced damage to MN9D cells induced by 6-OHDA. ICT increased SOD activity and TH expression and reduced ROS production and α-Syn expression. ICT promoted the translocation of Nrf2 from the cytoplasm to the nucleus and further increased the protein expression of HO-1. Conclusions: ICT protects against 6-OHDA-induced dopaminergic neuronal cell injury by attenuating oxidative stress, and the mechanism is related to modulate the activities of Nrf2, HO-1 protein, and SOD.
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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.