ArticleCellular and molecular neurobiology2021
Evodiamine Inhibits Lipopolysaccharide (LPS)-Induced Inflammation in BV-2 Cells via Regulating AKT/Nrf2-HO-1/NF-κB Signaling Axis.
Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Antitumor Effects of Evodiamine in Mice Model Experiments: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Combined Anti-Inflammatory Effects of Curcumin and Evodiamine: In Vitro Synergy, Docking, and Molecular Orbital Insights.International journal of molecular sciences · 2026Article
- Cardamonin ameliorates neuroinflammation in Parkinson's disease by regulating NF-κB signaling.Hereditas · 2026Article
- Protective Effects of Arecoline on LPS-Induced Neuroinflammation in BV2 Microglial Cells.International journal of molecular sciences · 2025Article
- Application of traditional Chinese medicine integrated therapy based on Tuina and herbal medicine in pediatric diarrhea.World journal of gastroenterology · 2025Review
- Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells.Current issues in molecular biology · 2025Article
- Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases.Cells · 2025Review
- Evodiamine encapsulated by hyaluronic acid modified zeolitic imidazolate framework-8 for tumor targeted therapy.Drug delivery and translational research · 2025Article
- Emodin alleviates intestinal ischemia-reperfusion injury through antioxidant stress, anti-inflammatory responses and anti-apoptosis effects via Akt-mediated HO-1 upregulation.Journal of inflammation (London, England) · 2024Article
- Evodiamine ameliorates intervertebral disc degeneration through the Nrf2 and MAPK pathways.Cytotechnology · 2024Article
- RTA-408 Regulates p-NF-κB/TSLP/STAT5 Signaling to Ameliorate Nociceptive Hypersensitivity in Chronic Constriction Injury Rats.Molecular neurobiology · 2024Article
- Evodiamine inhibits growth of vemurafenib drug-resistant melanoma via suppressing IRS4/PI3K/AKT signaling pathway.Journal of natural medicines · 2024Article
- Review
- Study on the Alleviating Effect and Potential Mechanism of Ethanolic Extract ofInternational journal of molecular sciences · 2023Article
- Elucidation of the relationship between evodiamine-induced liver injury and CYP3A4-mediated metabolic activation by UPLC-MS/MS analysis.Analytical and bioanalytical chemistry · 2023Article
- Is Nuclear Factor Erythroid 2-Related Factor 2 a Target for the Intervention of Cytokine Storms?Antioxidants (Basel, Switzerland) · 2023Review
- The Protective Effect of Zebularine, an Inhibitor of DNA Methyltransferase, on Renal Tubulointerstitial Inflammation and Fibrosis.International journal of molecular sciences · 2022Article
- Fraxetin alleviates microglia-mediated neuroinflammation after ischemic stroke.Annals of translational medicine · 2022Article
- Evodiamine Relieve LPS-Induced Mastitis by Inhibiting AKT/NF-κB p65 and MAPK Signaling Pathways.Inflammation · 2022Article
- Analgesic Alkaloids Derived From Traditional Chinese Medicine in Pain Management.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation is caused by excessive activation of microglia and plays an essential role in neurodegenerative diseases. After activation, microglia produce several kinds of inflammatory mediators, trigger an excessive inflammatory response, and ultimately destroy the surrounding neurons. Therefore, agents that inhibit neuroinflammation may be potential drug candidates for neurodegenerative diseases. Evodiamine (EV) has anti-inflammatory functions in peripheral tissues. However, whether EV exerts the same function in neuroinflammation is not known. In the present study, the aim was to explore whether EV attenuates microglial overactivation and therefore suppresses the development of neuroinflammation in lipopolysaccharide (LPS)-stimulated BV-2 cells. It was found that EV effectively inhibited expression of proinflammatory mediators (cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)) via AKT/Nrf2/HO-1 activation and suppressed NF-κB p65 phosphorylation. In addition, EV could suppress LPS-induced inflammatory response and loss of dopaminergic neuron in mouse mesencephalic neuron--glia cells. Hence, these findings demonstrate that EV suppresses neuroinflammation caused by overactivated microglia via regulating the AKT/Nrf2/HO-1/NF-κB signaling axis.
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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.