Evidence map›Paper›PMID 32399817›Full record

ArticleMolecular neurobiology2020

Tannic Acid Provides Neuroprotective Effects Against Traumatic Brain Injury Through the PGC-1α/Nrf2/HO-1 Pathway.

Mohd Salman, Heena Tabassum, Suhel Parvez

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 62 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

3 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.
Heena TabassumDivision of Biomedical Sciences, Indian Council of Medical Research, Ministry of Health and Family Welfare, Govt. of India, V. Ramalingaswamy Bhawan, P.O. Box No. 4911, New Delhi, 110029, India. tabassum.h@icmr.gov.in.
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 · INIndian Council of Medical Research · IN

Funding

Indian Council of Medical Research No. 3/1/2/4/Trauma/2019-NCD-1
6 · The paper itself

Abstract

The present research was conducted to elucidate a possible molecular mechanism related to neuromodulatory effects of tannic acid (TA) supplementation against traumatic brain injury (TBI) in a rodent model. Oxidative damage and neuroinflammation play a critical role in TBI and lead to behavioral alterations and neuronal dysfunction and death. These changes suggest a potential avenue in neurotherapeutic intervention. The aim of the present study was to investigate the neuroprotective effects of TA and potential mechanism of these effects in a controlled cortical impact injury model of TBI in Wistar rats that were treated with TA (50 mg/kg body weight. i.p.) before 30 min and 6 and 18 h after TBI. TBI-induced rats were examined after 24 h for behavioral dysfunction, Nissl stain, lipid peroxidation rate, glutathione level, activities of antioxidant enzymes (catalase, glutathione S-transferase, glutathione peroxidase, and superoxide dismutase), the expression level of 4-hydroxynonenal, pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-1 beta, as well as brain edema and immunoreactivity of glial fibrillary acidic protein. Results indicated that TA supplementation significantly modulated above mentioned alterations. Moreover, TA treatment effectively upregulated the protein expression of peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α) and nuclear factor-E2-related factor-2 (Nrf2) as well as mitochondrial transcription factor A and heme oxygenase-1 (HO-1) following TBI. Overall, our results suggest that TA effectively ameliorates the behavioral alterations, oxidative damage, mitochondrial impairment, and inflammation against TBI that may be attributed to activation of PGC-1α/Nrf-2/HO-1 signaling pathway.

Indexed as

AnimalsBrainBrain Injuries, TraumaticCatalaseGlutathione PeroxidaseHeme Oxygenase (Decyclizing)MaleMitochondriaNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, WistarSignal TransductionSuperoxide DismutaseCatalaseGlutathione PeroxidaseHeme Oxygenase (Decyclizing)Hmox1 protein, ratNeuroprotective AgentsNfe2l2 protein, ratNF-E2-Related Factor 2Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratSuperoxide DismutaseTanninsInflammationNrf2Oxidative stressPGC-1αTannic acidTraumatic brain injury

Identifiers

PMID32399817
OpenAlexW3025286369

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.