Impact of vildagliptin on vascular and fibrotic remodeling of myocardium in experimental diabetic cardiomyopathy.

Autor: Abdel-Hamid AAM; Department of Medical Histology and Cell Biology, Faculty of Medicine, Mansoura University, Egypt; Department of Anatomy, Taibah College of Medicine, Taibah University, Almadina Almonawara, Saudi Arabia. Electronic address: profahmadpasha@mans.edu.eg., Firgany AEL; Department of Medical Histology and Cell Biology, Faculty of Medicine, Mansoura University, Egypt; Department of Basic Medical Sciences, Unit of Anatomy, Unaizah College of Medicine, Qassim University, AlQassim, Saudi Arabia.
Jazyk: angličtina
Zdroj: Acta histochemica [Acta Histochem] 2020 Feb; Vol. 122 (2), pp. 151499. Date of Electronic Publication: 2019 Dec 28.
DOI: 10.1016/j.acthis.2019.151499
Abstrakt: The effect of dipeptidyl peptidase-4 inhibitors (DPP-4is) on myocardium in diabetic cardiomyopathy (DCM) remains a matter of debate. In the current study we investigated the effect of vildagliptin (VILDA, 3 mg/kg/d) on myocardium of DCM focusing on coronary microcirculation as well as on endothelial stress markers (ICAM and VCAM). We divided animals equally into 4 groups; nondiabetic (ND), VILDA per se, DCM and DCM + VILDA and their myocardium was evaluated for the fibro-vascular remodeling immunohistochemically as well as for molecular changes. VILDA had reversed the histological changes occurred in DCM including the disintegration, degeneration, and steatosis of cardiomyocytes with disappearance of the edema fluid. In addition VILDA significantly increased (p < 0.05) density of the coronary microcirculation and relieved endothelial stress. However, it did not prevent the development of fibrotic remodeling including the increased collagen deposition and the significantly upregulated (p < 0.05) corresponding genes. Therefore VILDA may have a positive impact on the microvascular remodeling, but not on fibrotic changes, in DCM.
Competing Interests: Declaration of Competing Interest There is no conflict of interest regarding the current article.
(Copyright © 2019 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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