ArticleIranian journal of basic medical sciences2021
Huperzine A protects against traumatic brain injury through anti-oxidative effects via the Nrf2-ARE pathway.
Article in Iranian journal of basic medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Alkaloids as Emerging Neuroprotective Agents for Neurodegenerative Disorders: Insights into Tryptanthrin and Its Derivatives.International journal of molecular sciences · 2026Review
- Advantages of nanocarriers for basic research in the field of traumatic brain injury.Neural regeneration research · 2024Review
- Intravitreal injection of Huperzine A promotes retinal ganglion cells survival and axonal regeneration after optic nerve crush.Frontiers in cellular neuroscience · 2023Article
- Nrf2 Activation: Involvement in Central Nervous System Traumatic Injuries. A Promising Therapeutic Target of Natural Compounds.International journal of molecular sciences · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTraumatic brain injury (TBI) is a prominent health problem worldwide and it may lead to cognitive dysfunction, disability, and even death. To date, there is no effective treatment for TBI. Our previous study showed that Huperzine A (HupA) improved cognitive function in a mouse model of TBI. However, the detailed mechanism of HupA remains unaddressed. In this study, we investigated the possible mechanism of the neuroprotective effect of HupA. MATERIALS AND
methodsC57BL/6 mice were randomly divided into 3 groups as sham, injured with vehicle treatment, and injured with HupA treatment groups. The Morris water maze task was used to evaluate the impairment of special learning and memory. Brain edema was as-sessed by measuring the wet weight to dry weight ratio. Malondialdehyde (MDA) and glutathione peroxidase (GPx) levels were measured for oxidative stress. Protein expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygen-ase-1(HO-1), and synaptophysin were detected by Western blot. The brain sections were stained with hematoxylin-eosin (H&E) for histology study.
resultsWe found that HupA therapy improved histology and cognitive functional outcomes after TBI. HupA reduced brain edema in TBI mice. furthermore, HupA inhibited ox-idative stress. HupA promoted nuclear factor erythroid 2-related factor 2 (Nrf2) nu-clear translocation and activated Nrf2 after TBI.
conclusionHupA protects against TBI through antioxidative effects via the Nrf2-ARE pathway.
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