Evidence map›Paper›PMID 24520409›Full record

ArticlePloS one2014

Acacetin inhibits glutamate release and prevents kainic acid-induced neurotoxicity in rats.

Tzu-Yu Lin, Wei-Jan Huang, Chia-Chan Wu, Cheng-Wei Lu, Su-Jane Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 15% of its field
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

15 citing papers in PubMed, 55 citations in OpenAlex.

  1. Volkameria (L.): A comprehensive review of its traditional medicine uses, phytochemistry and pharmacology.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  2. Treating Epilepsy with Natural Products: Nonsense or Possibility?Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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  10. Traditional uses and pharmacological properties ofJournal of traditional and complementary medicine · 2018
    Review
  11. Article
  12. Review
  13. Article
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  15. 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 at 4 institutions in 1 country.

Tzu-Yu LinDepartment of Anesthesiology, Far-Eastern Memorial Hospital, New Taipei, Taiwan ; Department of Mechanical Engineering, Yuan Ze University, New Taipei, Taiwan.
Wei-Jan HuangGraduate Institute of Pharmacognosy, Taipei Medical University, Taipei, Taiwan.
Chia-Chan WuDepartment of Anesthesiology, Far-Eastern Memorial Hospital, New Taipei, Taiwan.
Cheng-Wei LuDepartment of Anesthesiology, Far-Eastern Memorial Hospital, New Taipei, Taiwan ; Department of Mechanical Engineering, Yuan Ze University, New Taipei, Taiwan.
Su-Jane WangGraduate Institute of Basic Medicine, Fu Jen Catholic University, New Taipei, Taiwan.
Far Eastern Memorial Hospital · TWFu Jen Catholic University · TWTaipei Medical University · TWYuan Ze University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An excessive release of glutamate is considered to be a molecular mechanism associated with several neurological diseases that causes neuronal damage. Therefore, searching for compounds that reduce glutamate neurotoxicity is necessary. In this study, the possibility that the natural flavone acacetin derived from the traditional Chinese medicine Clerodendrum inerme (L.) Gaertn is a neuroprotective agent was investigated. The effect of acacetin on endogenous glutamate release in rat hippocampal nerve terminals (synaptosomes) was also investigated. The results indicated that acacetin inhibited depolarization-evoked glutamate release and cytosolic free Ca(2+) concentration ([Ca(2+)]C) in the hippocampal nerve terminals. However, acacetin did not alter synaptosomal membrane potential. Furthermore, the inhibitory effect of acacetin on evoked glutamate release was prevented by the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channel blocker known as ω-conotoxin MVIIC. In a kainic acid (KA) rat model, an animal model used for excitotoxic neurodegeneration experiments, acacetin (10 or 50 mg/kg) was administrated intraperitoneally to the rats 30 min before the KA (15 mg/kg) intraperitoneal injection, and subsequently induced the attenuation of KA-induced neuronal cell death and microglia activation in the CA3 region of the hippocampus. The present study demonstrates that the natural compound, acacetin, inhibits glutamate release from hippocampal synaptosomes by attenuating voltage-dependent Ca(2+) entry and effectively prevents KA-induced in vivo excitotoxicity. Collectively, these data suggest that acacetin has the therapeutic potential for treating neurological diseases associated with excitotoxicity.

Indexed as

4-AminopyridineAnimalsCalciumCalcium Channel BlockersCalcium ChannelsCell DeathFlavonesGlutamic AcidHippocampusKainic AcidMaleMembrane PotentialsMicrogliaNerve EndingsNeuronsNeurotoxins4-AminopyridineacacetinCalciumCalcium Channel BlockersCalcium ChannelsFlavonesGlutamic AcidKainic AcidNeurotoxinsPotassium ChlorideSodium

Identifiers

PMID24520409
PMCPMC3919813
OpenAlexW2020839833

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.