Evidence map›Paper›PMID 23209812›Full record

ArticlePloS one2012

Saikosaponin a mediates the anticonvulsant properties in the HNC models of AE and SE by inhibiting NMDA receptor current and persistent sodium current.

Yun-Hong Yu, Wei Xie, Yong Bao, Hui-Ming Li, San-Jue Hu, Jun-Ling Xing

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 46% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  4. Review
  5. Review
  6. Treating Epilepsy with Natural Products: Nonsense or Possibility?Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  7. Review
  8. Review
  9. Analysis of Medication Rule of Primary Epilepsy Based onEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  10. Review
  11. Chinese Herbal Medicine for Treating Epilepsy.Frontiers in neuroscience · 2021
    Review
  12. A comprehensive review and perspectives on pharmacology and toxicology of saikosaponins.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Saikosaponin a Enhances Transient Inactivating Potassium Current in Rat Hippocampal CA1 Neurons.Evidence-based complementary and alternative medicine : eCAM · 2013
    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

6 authors at 3 institutions in 1 country.

Yun-Hong YuDepartment of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guang Zhou, People's Republic of China.
Wei Xie
Yong Bao
Hui-Ming Li
San-Jue Hu
Jun-Ling Xing
Air Force Medical University · CNNanfang Hospital · CNLu'an First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is one of the most common neurological disorders, yet its treatment remains unsatisfactory. Saikosaponin a (SSa), a triterpene saponin derived from Bupleurum chinensis DC., has been demonstrated to have significant antiepileptic activity in a variety of epilepsy models in vivo. However, the electrophysiological activities and mechanisms of the antiepileptic properties of SSa remain unclear. In this study, whole-cell current-clamp recordings were used to evaluate the anticonvulsant activities of SSa in the hippocampal neuronal culture (HNC) models of acquired epilepsy (AE) and status epilepticus (SE). Whole-cell voltage-clamp recordings were used to evaluate the modulation effects of SSa on NMDA-evoked current and sodium currents in cultured hippocampal neurons. We found that SSa effectively terminated spontaneous recurrent epileptiform discharges (SREDs) in the HNC model of AE and continuous epileptiform high-frequency bursts (SE) in the HNC model of SE, in a concentration-dependent manner with an IC(50) of 0.42 µM and 0.62 µM, respectively. Furthermore, SSa significantly reduced the peak amplitude of NMDA-evoked current and the peak current amplitude of I(NaP). These results suggest for the first time that the inhibitions of NMDA receptor current and I(NaP) may be the underlying mechanisms of SSa's anticonvulsant properties, including the suppression of SREDs and SE in the HNC models of AE and SE. In addition, effectively abolishing the refractory SE implies that SSa may be a potential anticonvulsant candidate for the clinical treatment of epilepsy.

Indexed as

AnimalsAnticonvulsantsCells, CulturedElectrophysiologyEpilepsyHippocampusNeuronsOleanolic AcidRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSaponinsSodiumStatus EpilepticusAnticonvulsantsOleanolic AcidReceptors, N-Methyl-D-Aspartatesaikosaponin DSaponinsSodium

Identifiers

PMID23209812
PMCPMC3510157
OpenAlexW1997981393

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.