Evidence map›Paper›PMID 32922492›Full record

ArticleIranian journal of pharmaceutical research : IJPR2020

Exogenous Ghrelin Could Not Ameliorate 3,4-methylenedioxymethamphetamine-induced Acute Liver Injury in The Rat: Involved Mechanisms.

Ravieh Golchoobian, Fatemeh Nabavizadeh, Mehrdad Roghani, Alireza Foroumadi, Maryam Izad, Maryam Bahrami, Hafseh Fanaei

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of pharmaceutical research : IJPR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 98% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Time-Dependent Molecular Changes Following MDMA-Induced Nephrotoxicity.Iranian journal of pharmaceutical research : IJPR
    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 3 institutions in 1 country.

Ravieh GolchoobianDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Fatemeh NabavizadehDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mehrdad RoghaniNeurophysiology Research Center, Shahed University, Tehran, Iran.
Alireza ForoumadiDepartment of Medicinal Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Maryam IzadDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences Tehran, Iran.
Maryam BahramiDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Hafseh FanaeiDepartment of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Tehran University of Medical Sciences · IRAhvaz Jundishapur University of Medical Sciences · IRShahed University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MDMA (3,4-methylenedioxymethamphetamine, ecstasy) is often abused by youth as a recreational drug. MDMA abuse is a growing problem in different parts of the world. An important adverse consequence of the drug consumption is hepatotoxicity of different intensities. However, the underlying mechanism of this toxicity has not been completely understood. Ghrelin is a gut hormone with growth hormone stimulatory effect. It expresses in liver, albeit at a much lower level than in stomach, and exerts a hepatoprotective effect. In this study, we investigated hepatotoxicity effect of MDMA alone and its combination with ghrelin as a hepatoprotective agent. MDMA and MDMA+ ghrelin could transiently increase serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) followed by tissue necrosis. However, they could significantly decrease liver tumor necrosis factor-a (TNF-±) in both treatment groups. Unexpectedly, in MDMA treated rats, Bax, Bcl-xl, Bcl-2, Fas, Fas ligand (Fas-L), caspase 8, cytochrome c, caspase 3 gene expression, and DNA fragmentation were nearly unchanged. In addition, apoptosis in MDMA+ ghrelin group was significantly reduced when compared with MDMA treated animals. In all, MDMA could transiently increase serum transaminases and induce tissue necrosis and liver toxicity. Ghrelin, however, could not stop liver enzyme rise and MDMA hepatotoxicity. MDMA hepatotoxicity seems to be mediated via tissue necrosis than apoptotic and inflammatory pathways. Conceivably, ghrelin as an anti-inflammatory and anti-apoptotic agent may not protect hepatocytes against MDMA liver toxicity.

Indexed as

34-methylenedioxymethamphetamineApoptosisGhrelinHepatotoxicityNecrosisTNF-α

Identifiers

PMID32922492
PMCPMC7462488
OpenAlexW3012910213

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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.