Evidence map›Paper›PMID 32468441›Full record

ArticleCellular and molecular neurobiology2021

Melatonin Provides Neuroprotection Following Traumatic Brain Injury-Promoted Mitochondrial Perturbation in Wistar Rat.

Mohd Salman, Pooja Kaushik, Heena Tabassum, Suhel Parvez

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Mohd SalmanDepartment of Medical Elementology and Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, 110062, India.
Pooja KaushikDepartment of Medical Elementology and Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, 110062, India.
Heena TabassumDivision of Basic Medical Sciences, Indian Council of Medical Research, Ministry of Health and Family Welfare, Government of India, V. Ramalingaswamy Bhawan, P.O. Box No. 4911, New Delhi, 110029, India.
Suhel ParvezDepartment of Medical Elementology and Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, 110062, India. sparvez@jamiahamdard.ac.in.ORCID http://orcid.org/0000-0002-6318-6506
Jamia Hamdard · INGovernment of India · IN

Funding

Department of Science and Technology, Ministry of Science and Technology SR/CSI/PDF-76/ 2012Indian Council of Medical Research F.No.3/1/2/4/Trauma/2009-NCD-1Science and Engineering Research Board 2016/001070/HSUGC-DAE Consortium for Scientific Research, University Grants Commission F.No.-25-1/2014-15(BSR)/7-91/2017/(BSR
6 · The paper itself

Abstract

Excessive mitochondrial fission has been implicated in the etiology of neuronal cell death in traumatic brain injury (TBI). In the present study, we examined the efficacy of melatonin (Mel) as a neuroprotective agent against TBI-induced oxidative damage and mitochondrial dysfunction. We assessed the impact of Mel post-treatment (10 mg/kg b.wt., i.p.) at different time intervals in TBI-subjected Wistar rats. We found that the Mel treatment significantly attenuated brain edema, oxidative damage, mitochondrial fission, and promoted mitochondrial fusion. Additionally, Mel-treated rats showed restoration of mitochondrial membrane potential and oxidative phosphorylation with a concomitant reduction in cytochrome-c release. Further, Mel treatment significantly inhibited the translocation of Bax and Drp1 proteins to mitochondria in TBI-subjected rats. The restorative role of Mel treatment in TBI rats was supported by the mitochondrial ultra-structural analysis, which showed activation of mitochondrial fusion mechanism. Mel enhanced mitochondrial biogenesis by upregulation of PGC-1α protein. Our results demonstrated the remedial role of Mel in ameliorating mitochondrial dysfunctions that are modulated in TBI-subjected rats and provided support for mitochondrial-mediated neuroprotection as a putative therapeutic agent in the brain trauma.

Indexed as

NeuroprotectionAnimalsbcl-2-Associated X ProteinBehavior, AnimalBrain EdemaBrain Injuries, TraumaticCaspase 3Cytochromes cDynaminsMaleMelatoninMembrane Potential, MitochondrialMitochondriaMitochondrial DynamicsMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesbcl-2-Associated X ProteinCaspase 3Cytochromes cDnm1l protein, ratDynaminsF1F0-ATP synthaseMelatoninMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaDrp1MelatoninMitochondria dysfunctionNeuroprotectionRepairTraumatic brain injury

Identifiers

PMID32468441
PMCPMC11448575
OpenAlexW3029724038

What OpenQuestion holds

Textmetadata
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.