Evidence map›Paper›PMID 30737662›Full record

ArticleInflammation2019

Saroglitazar Deactivates the Hepatic LPS/TLR4 Signaling Pathway and Ameliorates Adipocyte Dysfunction in Rats with High-Fat Emulsion/LPS Model-Induced Non-alcoholic Steatohepatitis.

Noha F Hassan, Somaia A Nada, Azza Hassan, Mona R El-Ansary, Muhammad Y Al-Shorbagy, Rania M Abdelsalam

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Regression of hepatic fibrosis after pharmacological therapy for nonalcoholic steatohepatitis.World journal of gastrointestinal pharmacology and therapeutics · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Pharmaceutical biology · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Drugs for Non-alcoholic Steatohepatitis (NASH): Quest for the Holy Grail.Journal of clinical and translational hepatology · 2021
    Review
  19. Article
  20. Current and Emerging Approaches for Hepatic Fibrosis Treatment.Gastroenterology research and practice · 2021
    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

6 authors at 3 institutions in 1 country.

Noha F HassanDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Modern University for Technology and Information, Cairo, Egypt.
Somaia A NadaDepartment of Pharmacology and Toxicology, National Research Centre, Giza, Egypt.
Azza HassanDepartment of Pathology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
Mona R El-AnsaryDepartment of Biochemistry, Faculty of Pharmacy, Modern University for Technology and Information, Al-Mokattam, Cairo, Egypt. mona.el-Ansary@pharm.mti.edu.eg.ORCID http://orcid.org/0000-0002-7904-7914
Muhammad Y Al-ShorbagyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Rania M AbdelsalamDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Cairo University · EGModern University for Information and Technology · EGNational Research Centre · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The most epidemic liver disorder non-alcoholic steatohepatitis (NASH) is characterized by hepatic steatosis and inflammation with hepatocellular damage. Recently, it is predictable to be the extensive cause for liver transplantation. The absence of an approved therapeutic agent for NASH is the reason for investigating saroglitazar (SAR) which showed promising effects as a dual PPAR-α/γ agonist in recent studies on NASH. Here, we aimed to investigate the effect of SAR on NASH induced in rats by the administration of high-fat emulsion (HFE) and small doses of lipopolysaccharides (LPS) for 5 weeks. Rats were divided into three groups: negative control group (saline and standard rodent chow), model group (HFE(10 ml/kg/day, oral gavage) + LPS(0.5 mg/kg/week, i.p)), and SAR-treated group (HFE(10 ml/kg/day, oral gavage) + LPS(0.5 mg/kg/week, i.p.) + SAR(4 mg/kg/day, oral gavage) starting at week 3.Treatment with SAR successfully ameliorated the damaging effects of HFE with LPS, by counteracting body weight gain and biochemically by normalization of liver function parameters activity, glucose, insulin, homeostasis model of assessment (HOMA-IR) score, lipid profile levels, and histopathological examination. Significant changes in adipokine levels were perceived, resulting in a significant decline in serum leptin and tumor necrosis factor-α (TNF-α) level concurrent with adiponectin normalization. The positive effects observed for SAR on NASH are due to the downregulation of the LPS/TLR4 pathway, as indicated by the suppression of hepatic Toll-like receptor 4 (TLR4), NF-κB, TNF-α, and transforming growth factor-β1 (TGF-β1) expression. In conclusion, this work verified that SAR ameliorates NASH through deactivation of the hepatic LPS/TLR4 pathway and inhibition of adipocyte dysfunction.

Indexed as

AdipocytesAnimalsDown-RegulationLipopolysaccharidesLiverNon-alcoholic Fatty Liver DiseasePhenylpropionatesPyrrolesRatsSignal TransductionToll-Like Receptor 4LipopolysaccharidesPhenylpropionatesPyrrolessaroglitazarTlr4 protein, ratToll-Like Receptor 4adipocytelipopolysaccharideNASHPPAR-α/γ agonistsaroglitazartoll-like receptor 4

Identifiers

PMID30737662
OpenAlexW2914778832

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.