ArticleActa pharmacologica Sinica2016
Acetylcholinesterase-independent protective effects of huperzine A against iron overload-induced oxidative damage and aberrant iron metabolism signaling in rat cortical neurons.
Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Plant-mediated green nanoparticles: combining nanometal and biometabolite potential for Alzheimer's treatment.Biomedical engineering online · 2026Review
- Huperzine A improves neurological function in mice with intracerebral hemorrhage by alleviating neuroinflammation and ferroptosis.Scientific reports · 2026Article
- Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition.Acta biochimica et biophysica Sinica · 2024Article
- Microneedles: A Versatile Drug Delivery Carrier for Phytobioactive Compounds as a Therapeutic Modulator for Targeting Mitochondrial Dysfunction in the Management of Neurodegenerative Diseases.Current neuropharmacology · 2024Review
- Huperzine A-Liposomes Efficiently Improve Neural Injury in the Hippocampus of Mice with Chronic Intermittent Hypoxia.International journal of nanomedicine · 2023Article
- A Synopsis of Multitarget Potential Therapeutic Effects of Huperzine A in Diverse Pathologies-Emphasis on Alzheimer's Disease Pathogenesis.Neurochemical research · 2022Review
- Role of Cholinergic Signaling in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022Review
- Involvement of Hepcidin in Cognitive Damage Induced by Chronic Intermittent Hypoxia in Mice.Oxidative medicine and cellular longevity · 2021Article
- An optically active isochroman-2H-chromene conjugate potently suppresses neuronal oxidative injuries associated with the PI3K/Akt and MAPK signaling pathways.Acta pharmacologica Sinica · 2021Article
- Pharmacokinetics, excretion and metabolites analysis of DL0410, a dual‑acting cholinesterase inhibitor and histamine‑3 receptor antagonist.Molecular medicine reports · 2019Article
- Article
- Iron dysregulates APP processing accompanying with sAPPα cellular retention and β-secretase inhibition in rat cortical neurons.Acta pharmacologica Sinica · 2018Article
- Assessment of Enzyme Inhibition: A Review with Examples from the Development of Monoamine Oxidase and Cholinesterase Inhibitory Drugs.Molecules (Basel, Switzerland) · 2017Review
- [Role of mitophagy in neonatal rats with hypoxic-ischemic brain damage].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Article
- Isolation and characterization of phthalates from Brevibacterium mcbrellneri that cause cytotoxicity and cell cycle arrest.EXCLI journal · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimIron dyshomeostasis is one of the primary causes of neuronal death in Alzheimer's disease (AD). Huperzine A (HupA), a natural inhibitor of acetylcholinesterase (AChE), is a licensed anti-AD drug in China and a nutraceutical in the United Sates. Here, we investigated the protective effects of HupA against iron overload-induced injury in neurons.
methodsRat cortical neurons were treated with ferric ammonium citrate (FAC), and cell viability was assessed with MTT assays. Reactive oxygen species (ROS) assays and adenosine triphosphate (ATP) assays were performed to assess mitochondrial function. The labile iron pool (LIP) level, cytosolic-aconitase (c-aconitase) activity and iron uptake protein expression were measured to determine iron metabolism changes. The modified Ellman's method was used to evaluate AChE activity.
resultsHupA significantly attenuated the iron overload-induced decrease in neuronal cell viability. This neuroprotective effect of HupA occurred concurrently with a decrease in ROS and an increase in ATP. Moreover, HupA treatment significantly blocked the upregulation of the LIP level and other aberrant iron metabolism changes induced by iron overload. Additionally, another specific AChE inhibitor, donepezil (Don), at a concentration that caused AChE inhibition equivalent to that of HupA negatively, influenced the aberrant changes in ROS, ATP or LIP that were induced by excessive iron.
conclusionWe provide the first demonstration of the protective effects of HupA against iron overload-induced neuronal damage. This beneficial role of HupA may be attributed to its attenuation of oxidative stress and mitochondrial dysfunction and elevation of LIP, and these effects are not associated with its AChE-inhibiting effect.
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