Evidence map›Paper›PMID 42151222›Full record

ArticleScientific reports2026

Oleuropein attenuates cardiac fibrosis via modulation of TGF-β1/Smad pathway in diabetic cardiomyopathy rat model.

Lobna M Abdelrauf, Danira A Habashy, Nadia M Sharaf, Asmaa A El-Shafei, Lobna Kassem, Ragwa M Abdelghany

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Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Lobna M AbdelraufDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt. lobna.rauf@gmail.com.
Danira A HabashyDepartment of Clinical Pharmacy, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt.
Nadia M SharafDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt.
Asmaa A El-ShafeiDepartment of Medical Histology and Cell Biology, Faculty of Medicine, Cairo University, Giza, Egypt.
Lobna KassemDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt.
Ragwa M AbdelghanyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibrosis is a key pathological feature of diabetic cardiomyopathy (DCM), contributing to progressive cardiac dysfunction. Transforming growth factor beta-1 (TGF-β1), via Smad2/3 signaling pathway, promotes fibrotic gene expression. Oleuropein (OL), a major phenolic constituent of olive products, exhibits significant antioxidant properties and contributes to cardiovascular protection. This study aimed to investigate the anti-fibrotic effects of OL in a rat model of DCM and its modulation of the TGF-β1/Smad signaling pathway, using Losartan as a positive control. Thirty-two male Wistar rats were randomly assigned to four groups: control, DCM, DCM + OL (40 mg/kg), and DCM + Losartan (10 mg/kg). DCM was induced via high-fat diet (HFD) and a single low-dose streptozotocin (STZ) injection (40 mg/kg). Cardiac function was assessed by echocardiography. Histological evaluation included hematoxylin-eosin (H&E) and Masson trichrome staining. Cardiac biomarkers, oxidative stress markers, and fibrosis-related markers were analyzed using RT-qPCR, immunohistochemistry, and western blotting. DCM rats exhibited cardiac dysfunction and fibrosis. OL treatment significantly improved cardiac function, reduced collagen and fibronectin (FN) deposition, and downregulated TGF-β1, Smad2/3, α-smooth muscle actin (α-SMA), collagen types I/III, matrix metalloproteinases-2/9 (MMPs), and tissue inhibitor of metalloproteinases-1 (TIMP-1), while enhancing Smad7 expression. Besides, OL demonstrated notable antioxidant and antidiabetic effects. In conclusion, OL alleviates cardiac fibrosis and dysfunction in DCM, potentially through modulation of the TGF-β1/Smad signaling, highlighting its therapeutic promise in diabetic cardiac complications.

Indexed as

Diabetic CardiomyopathiesIridoidsSignal TransductionSmad ProteinsTransforming Growth Factor beta1AnimalsDiabetes Mellitus, ExperimentalDisease Models, AnimalFibrosisIridoid GlucosidesMaleMyocardiumOxidative StressRatsRats, WistarSmad2 ProteinIridoid GlucosidesIridoidsoleuropeinSmad2 ProteinSmad2 protein, ratSmad3 ProteinSmad ProteinsTransforming Growth Factor beta1Cardiac fibrosisDiabetic cardiomyopathyOleuropeinTGF-β1/Smad signaling

Identifiers

PMID42151222
PMCPMC13184247

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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.