Evidence map›Paper›PMID 31512113›Full record

ArticleNeurochemical research2019

Sodium Valproate Reduces Neuronal Apoptosis in Acute Pentylenetetrzole-Induced Seizures via Inhibiting ER Stress.

Jie Fu, Lilei Peng, Weijun Wang, Haiping He, Shan Zeng, Thomas C Chen, Yangmei Chen

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05881928 (Effect of Adding Lamotrigine to Sodium Valproate in Childhood Epilepsy), which is not on this map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 22% 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.

NCT05881928 phase4unknown statusnot on this mapstarted 2024, after this paper: background citation

Effect of Adding Lamotrigine to Sodium Valproate in Childhood Epilepsy: Clinicolabratory Study

TypeinterventionalSponsorAssiut UniversityRan2024 to 2025Enrolled50ConditionsEpilepsy, Lamotrigine, Sodium Valproate Adverse ReactionArmsSodium Valproate 500 Mg Prolonged-Release Oral Tablet, Lamotrigine, E.E.G
3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. FAM134B-Mediated ER-Phagy in MgNeurochemical research · 2021
    Article
  8. 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

7 authors at 4 institutions in 2 countries.

Jie FuDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Lilei PengDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Weijun WangDepartments of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
Haiping HeDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Shan ZengDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Thomas C ChenDepartments of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. thomascc246@gmail.com.
Yangmei ChenDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. chenym1997@cqmu.edu.cn.
Neurological Surgery · USAffiliated Hospital of Southwest Medical University · CNDalian Medical University · CNUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress has been indicated to be involved in the pathogenesis of epilepsy. Sodium valproate (VPA), one of the most commonly used antiepileptic drugs, is reported to regulate ER stress in many neurological diseases. However, the effect of VPA on ER stress in epilepsy remains unclear. The current study was performed to investigate the role of ER stress in the neuroprotection of VPA against seizure induced by pentylenetetrzole (PTZ). Our results showed that VPA treatment could inhibit the increased expressions of ER stress proteins (GRP78 and CHOP), and significantly reduce neuronal apoptosis in the PTZ-induced experimental seizure model. In addition, Salubrinal, an ER stress inhibitor, was used as a positive control, and exhibited neuroprotective effects via inhibiting excessive ER stress in the seizure model, which further supported that the inhibition in ER stress by VPA treatment could exert neuroprotection in seizures. In summary, our work demonstrated for the first time that ER stress was involved in the neuroprotective potential of VPA for seizures.

Indexed as

AnimalsAnticonvulsantsApoptosisCinnamatesEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHeat-Shock ProteinsHippocampusMaleMice, Inbred C57BLNeuroprotective AgentsPentylenetetrazoleSeizuresThioureaTranscription Factor CHOPValproic AcidAnticonvulsantsCinnamatesDdit3 protein, mouseEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHspa5 protein, mouseNeuroprotective AgentsPentylenetetrazolesalubrinalThioureaTranscription Factor CHOPValproic AcidEpilepsyER stressNeuronal apoptosisPentylenetetrazoleSodium valproate

Identifiers

PMID31512113
OpenAlexW2972811737

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.