Evidence map›Paper›PMID 37310644›Full record

ArticleInflammation2023

Acetyl-11-Keto-Beta-Boswellic Acid Has Therapeutic Benefits for NAFLD Rat Models That Were Given a High Fructose Diet by Ameliorating Hepatic Inflammation and Lipid Metabolism.

Reza Ataei Kachouei, Alireza Doagoo, Maral Jalilzadeh, Seyyed Hossein Khatami, Shima Rajaei, Ali Jahanbazi Jahan-Abad, Farzaneh Salmani, Roya Pakrad, Somayeh Mahmoodi Baram, Mitra Nourbakhsh and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Frankincense (Current issues in molecular biology · 2024
    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

17 authors at 4 institutions in 2 countries.

Reza Ataei KachoueiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Alireza DoagooDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Maral JalilzadehScience and Research Branch, Islamic Azad University, Tehran, Iran.
Seyyed Hossein KhatamiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Shima RajaeiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Ali Jahanbazi Jahan-AbadDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Farzaneh SalmaniDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Roya PakradDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Somayeh Mahmoodi BaramClinical Trial Department, Behbalin Inc, Tehran, Iran.
Mitra NourbakhshDepartment of Clinical Biochemistry, School of Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran.
Mohammad-Amin AbdollahifarDepartment of Biology and Anatomy, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Hojjat Allah AbbaszadehLaser Application in Medical Sciences Research Center, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Shokoofeh NooriDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Mitra RezaeiDepartment of Pathology, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Meisam MahdaviDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Mohammad Reza ShahmohammadiFunctional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.
Saeed KarimaDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran. saeed.karima@sbmu.ac.ir.
Shahid Beheshti University of Medical Sciences · IRIran University of Medical Sciences · IRIslamic Azad University, Science and Research Branch · IRUniversity of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetyl-11-keto-beta-boswellic acid (AKBA), a potent anti-inflammatory compound purified from Boswellia species, was investigated in a preclinical study for its potential in preventing and treating non-alcoholic fatty liver disease (NAFLD), the most common chronic inflammatory liver disorder. The study involved thirty-six male Wistar rats, equally divided into prevention and treatment groups. In the prevention group, rats were given a high fructose diet (HFrD) and treated with AKBA for 6 weeks, while in the treatment group, rats were fed HFrD for 6 weeks and then given a normal diet with AKBA for 2 weeks. At the end of the study, various parameters were analyzed including liver tissues and serum levels of insulin, leptin, adiponectin, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor beta (TGF-β), interferon gamma (INF-ϒ), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α). Additionally, the expression levels of genes related to the inflammasome complex and peroxisome proliferator-activated receptor gamma (PPAR-ϒ), as well as the levels of phosphorylated and non-phosphorylated AMP-activated protein kinase alpha-1 (AMPK-α1) protein, were measured. The results showed that AKBA improved NAFLD-related serum parameters and inflammatory markers and suppressed PPAR-ϒ and inflammasome complex-related genes involved in hepatic steatosis in both groups. Additionally, AKBA prevented the reduction of the active and inactive forms of AMPK-α1 in the prevention group, which is a cellular energy regulator that helps suppress NAFLD progression. In conclusion, AKBA has a beneficial effect on preventing and avoiding the progression of NAFLD by preserving lipid metabolism, improving hepatic steatosis, and suppressing liver inflammation.

Indexed as

Non-alcoholic Fatty Liver DiseaseAMP-Activated Protein KinasesAnimalsDietFructoseInflammasomesInflammationLipid MetabolismLiverMalePeroxisome Proliferator-Activated ReceptorsRatsRats, WistarTriterpenesacetyl-11-ketoboswellic acidAMP-Activated Protein KinasesFructoseInflammasomesPeroxisome Proliferator-Activated ReceptorsTriterpenesAcetyl-11-keto-beta-boswellic acid (AKBA)AMP-activated protein kinase (AMPK)InflammasomeNon-alcoholic fatty liver disease (NAFLD)Peroxisome proliferator-activated receptor gamma (PPAR-ϒ)

Identifiers

PMID37310644
OpenAlexW4380422972

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.