Evidence map›Paper›PMID 38549169›Full record

ArticleBMC pharmacology & toxicology2024

Effects of nicotine on microRNA-124 expression in bile duct ligation-induced liver fibrosis in rats.

Khalil Hajiasgharzadeh, Parviz Shahabi, Elham Karimi-Sales, Mohammad Reza Alipour

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Combining sorafenib andIranian journal of basic medical sciences · 2026
    Article
  3. Review
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 1 institution in 1 country.

Khalil HajiasgharzadehStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. hajiasgharzadeh@tbzmed.ac.ir.
Parviz ShahabiDepartment of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Elham Karimi-SalesDepartment of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad Reza AlipourStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. alipourmr@tbzmed.ac.ir.
Tabriz University of Medical Sciences · IR

Funding

Stem Cell Research Center, Tabriz University of Medical Sciences 72284
6 · The paper itself

Abstract

backgroundNicotine, the main compound of smoking may exert its effects by changing the expression of microRNAs (miRNAs). This study was conducted to further investigate the molecular mechanisms of miRNA-dependent effects of nicotine in an animal model of liver fibrosis.

methodsThe bile duct ligation (BDL) approach was used to create a model of liver fibrosis. Twenty-four male Wistar rats were used in the study. The effects of nicotine administration on miRNA-124 expression, as well as alpha-smooth muscle actin (liver fibrosis marker) and chemokine ligand 2 (an inflammatory chemokine), were investigated using RT-qPCR. In addition, the mRNA and protein expression of signal transducer and activator of transcription 3 (STAT-3; as a potential target for miRNA-124) were investigated by RT-qPCR and immunofluorescence, respectively. Liver enzyme activity levels were measured using a colorimetric assay. In addition, the effects of nicotine on the process of liver fibrosis were investigated with histological studies.

resultsThe development of liver fibrosis in BDL rats and nicotine administration led to a decrease in miRNA-124 expression. The decrease in the expression is accompanied by the increase in the expression of fibrotic and proinflammatory genes. Also, an increase in STAT-3 mRNA and protein expression was observed in the fibrotic rats that received nicotine. In addition, the significant increase in bilirubin and liver enzymes in fibrotic rats worsens with nicotine administration. The results of histological studies also confirm these results.

conclusionConsidering that miRNA-124 is an anti-inflammatory miRNA, it can be concluded that the decrease in its expression due to nicotine exposure leads to an increase in inflammatory processes and subsequently to an increase in liver fibrosis.

Indexed as

LiverMicroRNAsAnimalsBile DuctsChemokinesDisease Models, AnimalFibrosisLiver CirrhosisMaleNicotineRatsRats, WistarRNA, MessengerChemokinesMicroRNAsMIRN124 microRNA, ratNicotineRNA, MessengerBile duct ligationInflammationLiver fibrosisMicroRNA-124Nicotine

Identifiers

PMID38549169
PMCPMC10976767
OpenAlexW4393277235

What Socratic holds

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LicenceCC BY
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 Socratic graph.