Evidence map›Paper›PMID 28748496›Full record

ArticleMetabolic brain disease2017

Huperzine A alleviates neuroinflammation, oxidative stress and improves cognitive function after repetitive traumatic brain injury.

Zhengrong Mei, Peiying Zheng, Xiangping Tan, Ying Wang, Bing Situ

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Article
  2. Review
  3. Natural Molecules for Brain Health and Resilience.International journal of molecular sciences · 2026
    Review
  4. Neuroprotective Effects of Huperzine B andAdvances in pharmacological and pharmaceutical sciences · 2026
    Article
  5. Article
  6. Nutrients · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Zhengrong MeiDepartment of Pharmacy, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong Province, 510150, People's Republic of China.
Peiying ZhengDepartment of Pharmacy, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong Province, 510150, People's Republic of China.
Xiangping TanDepartment of Pharmacy, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong Province, 510150, People's Republic of China.
Ying WangDepartment of Pharmacy, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong Province, 510150, People's Republic of China.
Bing SituDepartment of Pharmacy, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong Province, 510150, People's Republic of China. 646133313@qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) may trigger secondary injury cascades including endoplasmic reticulum stress, oxidative stress, and neuroinflammation. Unfortunately, there are no effective treatments targeting either primary or secondary injuries that result in long-term detrimental consequences. Huperzine A (HupA) is a potent acetylcholinesterase inhibitor (AChEI) that has been used treatment of Alzheimer's disease (AD). This study aimed to explore the neuroprotective effects of HupA in TBI and its possible mechanisms. Repetitive mild closed head injury (CHI) model was used to mimic concussive TBI. Mice were randomly assigned into three groups including sham, vehicle-treated and HupA-treated injured mice. The HupA was given at dose of 1.0 mg/kg/day and was initiated 30 min after the first injury, then administered daily for a total of 30 days. The neuronal functions including motor functions, emotion-like behaviors, learning and memory were tested. Axonal injury, reactive oxygen species (ROS), and neuroinflammation were examined as well. The results showed that injured mice treated with HupA had significant improvement in Morris water maze performance compared with vehicle-treated injured mice. HupA treatment significantly attenuated markers of neuroinflammation and oxidative stress in the injured mice. Taken together, HupA was effective in reducing neuroinflammation, oxidative stress and behavioral recovery after TBI. HupA is a promising candidate for treatment of TBI.

Indexed as

AlkaloidsAnimalsBehavior, AnimalBrain Injuries, TraumaticCognitionEncephalitisLearningMemoryMiceMotor ActivityNeuroprotective AgentsOxidative StressReactive Oxygen SpeciesSesquiterpenesAlkaloidshuperzine ANeuroprotective AgentsReactive Oxygen SpeciesSesquiterpenesHuperzine ANeuroinflammationNueroprotectionOxidative stressTraumatic brain injury

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Registered trials

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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.