Evidence map›Paper›PMID 28447311›Full record

ArticleMolecular neurobiology2018

Attenuation of Glutamate-Induced Excitotoxicity by Withanolide-A in Neuron-Like Cells: Role for PI3K/Akt/MAPK Signaling Pathway.

Nawab John Dar, Naresh Kumar Satti, Prabhu Dutt, Abid Hamid, Muzamil Ahmad

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.7field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

  1. Antioxidants (Basel, Switzerland) · 2026
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  15. International journal of molecular sciences · 2021
    Review
  16. Engineering ofBiomolecules · 2021
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  19. Review
  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 at 1 institution in 1 country.

Nawab John DarNeuropharmacology Laboratory, CSIR-Indian Institute of Integrative Medicine, Sanat Nagar, Srinagar, India.
Naresh Kumar SattiNatural Product Chemistry Division, Indian Institute of Integrative Medicine-CSIR, Canal Road, Jammu, India.
Prabhu DuttNatural Product Chemistry Division, Indian Institute of Integrative Medicine-CSIR, Canal Road, Jammu, India.
Abid HamidCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Canal Road, Jammu, India. ahdar@iiim.ac.in.
Muzamil AhmadNeuropharmacology Laboratory, CSIR-Indian Institute of Integrative Medicine, Sanat Nagar, Srinagar, India. mzmils@gmail.com.ORCID http://orcid.org/0000-0003-1066-1817
Indian Institute of Integrative Medicine · IN

Funding

Department of Biotechnology , Ministry of Science and Technology (BT/PR/3140/PBD/17/656/2009)Department of Biotechnology , Ministry of Science and Technology GAP1161
6 · The paper itself

Abstract

Glutamate-induced excitotoxicity is one of the major underlying mechanisms for neurodegenerative diseases. Efforts are being made to treat such conditions with an array of natural compounds that can modulate the release of glutamate or the underlying mechanisms associated with it. Withania somnifera extract has potent pharmacologic activity similar to that of Korean Ginseng tea and is used to treat several neuronal disorders. However, to date, little efforts have been made to evaluate individual constituents of this plant for neurodegenerative disorders. Present study was carried out to investigate withanolide-A, one of the active constituents of Withania somnifera against glutamate-induced excitotoxicity in retinoic acid differentiated Neuro2a neuroblastoma cells. The results indicated that glutamate treatment for 2 h induced death in cells that was significantly attenuated by pre-treatment with MK-801 (specific NMDA receptor antagonist) and different concentrations of withanolide-A. Withanolide-A abated the glutamate-induced influx of intracellular calcium and excessive ROS production significantly. Further on, glutamate treatment resulted in increased levels of pro-apoptotic and decreased levels of anti-apoptotic proteins, and these protein levels were normalized by various doses of withanolide-A. All of these protective effects were partly due to inhibition of MAPK family proteins and activation of PI3K/Akt signaling. Thus, our results suggest that withanolide-A may serve as potential neuroprotective agent.

Indexed as

Animalsbcl-2-Associated X ProteinBH3 Interacting Domain Death Agonist ProteinCalciumCell DeathCell DifferentiationCell Line, TumorGlutamic AcidIntracellular SpaceMAP Kinase Signaling SystemMiceModels, BiologicalNeuronsNeurotoxinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktbcl-2-Associated X ProteinBH3 Interacting Domain Death Agonist ProteinCalciumGlutamic AcidNeurotoxinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTumor Suppressor Protein p53WithanolidesGlutamateIntracellular calciumMAPK and PI3K/AktNMDAROSWithania somniferaWithanolide-A

Identifiers

PMID28447311
OpenAlexW2609408991

What OpenQuestion holds

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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.