Evidence map›Paper›PMID 37503477›Full record

ArticleCureus2023

Exploring the Therapeutic Potential of Apigenin in Obesity-Associated Fibrinolytic Dysfunction: Insights From an Animal Study.

Hasan H Qadi, Mohamed A Bendary, Safa Y Almaghrabi, Mohammed Alameen F Zaher, Mohamed M Karami, Ahmed M Alsehli, Omar Babateen, Ahmad F Arbaeen, Abdulhadi S Burzangi, Mohammed A Bazuhair

Open access · diamondAbstract read
In one paragraph

Article in Cureus, 2023. 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
1.2field-weighted citation impact, top 22% 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, 5 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

10 authors at 1 institution in 2 countries.

Hasan H QadiDepartment of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Mohamed A BendaryDepartment of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Safa Y AlmaghrabiDepartment of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Mohammed Alameen F ZaherDepartment of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Mohamed M KaramiDepartment of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Ahmed M AlsehliDepartment of Clinical Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Omar BabateenDepartment of Physiology, Faculty of Medicine, Umm Al-Qura University, Makkah, SAU.
Ahmad F ArbaeenDepartment of Laboratory Medicine, Faculty of Applied Medical Sciences, Umm Al-Qura University, Makkah, SAU.
Abdulhadi S BurzangiDepartment of Clinical Pharmacology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
Mohammed A BazuhairDepartment of Clinical Pharmacology, Faculty of Medicine, King Abdulaziz University, Jeddah, SAU.
King Abdulaziz University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionObesity (Obe) is a chronic metabolic disorder usually complicated by impaired fibrinolytic activity. Apigenin (Api) is one of the flavonoids that have anti-adiposity effects. This study aimed to explore the therapeutic potential of Api in high-fat diet (HFD)-induced obese rats.

methodsTwenty-four Wistar adult male rats were randomly allocated into control group, supplemented with a normal pellet diet (NPD); Api group, supplemented with Api (10 mg/kg) for eight weeks; Obe group, obesity was induced by feeding HFD for eight weeks; and Obe/Api group, obese rats supplemented with Api for eight weeks. Body mass index (BMI), homeostatic model assessment of insulin resistance (HOMA-IR), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), total superoxide dismutase (t-SOD) activity, and plasminogen activator inhibitor-1 (PAI-1) were measured.

resultsCompared to the control group, Obe group exhibited a significant increase in BMI, HOMA-IR, TNF-α, MDA, and PAI-1. These results were also associated with a significant decrease in serum t-SOD activity. Supplementation of Api alleviated the measured deteriorated parameters and ameliorated visceral adiposity in obese rats.

conclusionThis study provides compelling evidence regarding a promising role for Api in ameliorating the impairment of fibrinolytic activity in an Obe animal model. The observed effects are likely mediated through Api's anti-obesity properties, as well as its indirect modulation of PAI-1, oxidative stress, and inflammation. Future clinical studies are recommended that may make benefit of the preclinical therapeutic use of apigenin in obesity-associated fibrinolytic dysfunctions.

Indexed as

apigeninfibrinolysisinflammationobesityoxidative stressplasminogen activator inhibitor-1

Identifiers

PMID37503477
PMCPMC10370825
OpenAlexW4381989108

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.