Evidence map›Paper›PMID 31773435›Full record

ArticleMetabolic brain disease2020

Effect of cholestasis and NeuroAid treatment on the expression of Bax, Bcl-2, Pgc-1α and Tfam genes involved in apoptosis and mitochondrial biogenesis in the striatum of male rats.

Mohammad Nasehi, Sepehr Torabinejad, Mehrdad Hashemi, Salar Vaseghi, Mohammad-Reza Zarrindast

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In one paragraph

Article in Metabolic brain disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

5 authors at 2 institutions in 1 country.

Mohammad NasehiCognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences, Islamic Azad University, P.O. Box 13145-784, Tehran, Iran. Nasehi@iricss.org.
Sepehr TorabinejadDepartment of Genetics, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Mehrdad HashemiDepartment of Genetics, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Salar VaseghiCognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences, Islamic Azad University, P.O. Box 13145-784, Tehran, Iran.
Mohammad-Reza ZarrindastDepartment of Pharmacology School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Islamic Azad University Medical Branch of Tehran · IRInstitute for Cognitive Science Studies · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholestasis means impaired bile synthesis or secretion. In fact, it is a bile flow reduction following Bile Duct Ligation (BDL). Cholestasis has a main role in necrosis and apoptosis. Apoptosis is a form of programmed cell death that has intrinsic and extrinsic pathways. The intrinsic pathway is mediated by Bcl-2 (B cell lymphoma-2) proteins which integrate death and survival signals. Bcl-2 has anti-apoptotic and Bax has pro-apoptotic effects. Also, striatum is one of the brain regions that has high expressions of Bcl-2 proteins. Moreover, Tfam and Pgc-1α are involved in mitochondrial biogenesis. On the other hand, NeuroAid, is a drug that has neuroprotective and anti-apoptosis effects. In this study, using quantitative PCR, we measured the expression of all these genes in the striatum of male rats following BDL and NeuroAid administration. Results showed, BDL increased the expression of Bax and Tfam and decreased the expression of Bcl-2. NeuroAid restored the effect of BDL on the expression of Bax, while did not alter the effect of BDL on Bcl-2. In addition, it increased the expression of Tfam that was previously elevated by BDL and raised the expression of Tfam in normal rats. Both BDL and NeuroAid, had no effect on Pgc-1α. In conclusion, cholestasis increased the expression of Bax and decreased the expression of Bcl-2, and this effect may have related to enhanced susceptibility of mitochondrial pathways following oxidative stress. Tfam expression was increased following cholestasis and this effect may have related to cellular compensatory mechanisms against high accumulation of free radicals or mitochondrial biogenesis failure. Furthermore, NeuroAid may play a role against apoptosis and can be used to increase mitochondrial biogenesis.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCholestasisCorpus StriatumDrugs, Chinese HerbalGene ExpressionMaleOrganelle BiogenesisPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProto-Oncogene Proteins c-bcl-2RatsRats, WistarTranscription FactorsTreatment OutcomeBax protein, ratbcl-2-Associated X ProteinBcl2 protein, ratDrugs, Chinese HerbalNeuroaidPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratProto-Oncogene Proteins c-bcl-2Tfam protein, ratTranscription FactorsBaxBcl-2CholestasisNeuroAidPgc-1αTfam

Identifiers

PMID31773435
OpenAlexW2989583942

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.