ArticleInternational journal of molecular sciences2018
Pharmacological Basis for the Use of Evodiamine in Alzheimer's Disease: Antioxidation and Antiapoptosis.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- Exploring Mechanistic Targets ofInternational journal of molecular sciences · 2026Article
- Cardamonin ameliorates neuroinflammation in Parkinson's disease by regulating NF-κB signaling.Hereditas · 2026Article
- Mitochondrial quality control disorder in neurodegenerative disorders: Potential and advantages of traditional Chinese medicines.Journal of pharmaceutical analysis · 2025Review
- Euodiae Fructus: a review of botany, application, processing, phytochemistry, quality control, pharmacology, and toxicology.Frontiers in pharmacology · 2025Review
- Evodiamine: A Extremely Potential Drug Development Candidate of Alkaloids fromInternational journal of nanomedicine · 2024Review
- Chlorambucil-Bearing Hybrid Molecules in the Development of Potential Anticancer Agents.Molecules (Basel, Switzerland) · 2023Review
- Traditional Chinese medicine Euodiae Fructus: botany, traditional use, phytochemistry, pharmacology, toxicity and quality control.Natural products and bioprospecting · 2023Review
- Development of a new drug candidate for the inhibition of Lassa virus glycoprotein and nucleoprotein by modification of evodiamine as promising therapeutic agents.Frontiers in microbiology · 2023Article
- Protection against ulcerative colitis and colorectal cancer by evodiamine via anti‑inflammatory effects.Molecular medicine reports · 2022Article
- Discovery of an evodiamine derivative for PI3K/AKT/GSK3β pathway activation and AD pathology improvement in mouse models.Frontiers in molecular neuroscience · 2022Article
- Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases.Frontiers in pharmacology · 2022Review
- Mitochondria Related Cell Death Modalities and Disease.Frontiers in cell and developmental biology · 2022Review
- [Cytotoxicity and underlying mechanism of evodiamine in HepG2 cells].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2021Article
- Neuroprotective Studies of Evodiamine in an Okadaic Acid-Induced Neurotoxicity.International journal of molecular sciences · 2021Article
- Article
- Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling in U251 cells and APP/PS1 mice.Molecular medicine reports · 2021Article
- Anti-Inflammatory and Tau Phosphorylation-Inhibitory Effects of Eupatin.Molecules (Basel, Switzerland) · 2020Article
- Forsythoside B attenuates memory impairment and neuroinflammation via inhibition on NF-κB signaling in Alzheimer's disease.Journal of neuroinflammation · 2020Article
- An Indole Alkaloid Extracted fromGastroenterology research and practice · 2020Article
- MST1 Regulates Neuronal Cell Death via JNK/Casp3 Signaling Pathway in HFD Mouse Brain and HT22 Cells.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evodiamine (Evo), a major alkaloid compound isolated from the dry unripened fruit of Evodia fructus, has a wide range of pharmacological activities. The present study sought to explore the neuroprotective effects of Evo in l-glutamate (l-Glu)-induced apoptosis of HT22 cells, and in a d-galactose and aluminum trichloride-developed Alzheimer’s disease (AD) mouse model. Evo significantly enhanced cell viability, inhibited the accumulation of reactive oxygen species, ameliorated mitochondrial function, increased the B-cell lymphoma-2 protein content, and inhibited the high expression levels of Bax, Bad, and cleaved-caspase-3 and -8 in l-Glu-induced HT22 cells. Evo also enhanced the phosphorylation activities of protein kinase B and the mammalian target of rapamycin in the l-Glu-induced HT22 cells. In the AD mouse model, Evo reduced the aimless and chaotic movements, reduced the time spent in the central area in the open field test, and decreased the escape latency time in the Morris water maze test. Evo reduced the deposition of amyloid beta 42 (Aβ42) in the brain, and increased the serum level of Aβ42, but showed no significant effects on Aβ40. In addition, six weeks of Evo administration significantly suppressed oxidative stress by modulating the related enzyme levels. In the central cholinergic system of AD mice, Evo significantly increased the serum levels of acetylcholine and choline acetyltransferase and decreased the level of acetylcholinesterase in the serum, hypothalamus, and brain. Our results provide experimental evidence that Evo can serve as a neuroprotective candidate for the prevention and/or treatment of neurodegenerative diseases.
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