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Nutrients
Volume 10
Issue 10
10.3390/nu10101549
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Article

Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression

by
Putcharawipa Maneesai
1,2,
Sarawoot Bunbupha
3,
Prapassorn Potue
1,
Thewarid Berkban
3,
Upa Kukongviriyapan
1,2,
Veerapol Kukongviriyapan
4,
Parichat Prachaney
2,5 and
Poungrat Pakdeechote
1,2,*
1
Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand
2
Cardiovascular Research Group, Khon Kaen University, Khon Kaen 40002, Thailand
3
Faculty of Medicine, Mahasarakham University, Maha Sarakham 44000, Thailand
4
Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand
5
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand
*
Author to whom correspondence should be addressed.
Nutrients 2018, 10(10), 1549; https://doi.org/10.3390/nu10101549
Received: 21 September 2018 / Revised: 12 October 2018 / Accepted: 18 October 2018 / Published: 19 October 2018
(This article belongs to the Special Issue Nutrients Intake and Hypertension)
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Abstract

Hesperidin is a major flavonoid isolated from citrus fruits that exhibits several biological activities. This study aims to evaluate the effect of hesperidin on cardiovascular remodeling induced by n-nitro l-arginine methyl ester (l-NAME) in rats. Male Sprague-Dawley rats were treated with l-NAME (40 mg/kg), l-NAME plus hesperidin (15 mg/kg), hesperidin (30 mg/kg), or captopril (2.5 mg/kg) for five weeks (n = 8/group). Hesperidin or captopril significantly prevented the development of hypertension in l-NAME rats. l-NAME-induced cardiac remodeling, i.e., increases in wall thickness, cross-sectional area (CSA), and fibrosis in the left ventricular and vascular remodeling, i.e., increases in wall thickness, CSA, vascular smooth muscle cells, and collagen deposition in the aorta were attenuated by hesperidin or captopril. These were associated with reduced oxidative stress markers, tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta 1 (TGF-β1), and enhancing plasma nitric oxide metabolite (NOx) in l-NAME treated groups. Furthermore, up-regulation of tumor necrosis factor receptor type 1 (TNF-R1) and TGF- β1 protein expression and the overexpression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) was suppressed in l-NAME rats treated with hesperidin or captopril. These data suggested that hesperidin had cardioprotective effects in l-NAME hypertensive rats. The possible mechanism may involve antioxidant and anti-inflammatory effects. View Full-Text
Keywords: hesperidin; l-NAME; cardiovascular remodeling; oxidative stress; inflammation hesperidin; l-NAME; cardiovascular remodeling; oxidative stress; inflammation
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
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MDPI and ACS Style

Maneesai, P.; Bunbupha, S.; Potue, P.; Berkban, T.; Kukongviriyapan, U.; Kukongviriyapan, V.; Prachaney, P.; Pakdeechote, P. Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression. Nutrients 2018, 10, 1549. https://doi.org/10.3390/nu10101549

AMA Style

Maneesai P, Bunbupha S, Potue P, Berkban T, Kukongviriyapan U, Kukongviriyapan V, Prachaney P, Pakdeechote P. Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression. Nutrients. 2018; 10(10):1549. https://doi.org/10.3390/nu10101549

Chicago/Turabian Style

Maneesai, Putcharawipa, Sarawoot Bunbupha, Prapassorn Potue, Thewarid Berkban, Upa Kukongviriyapan, Veerapol Kukongviriyapan, Parichat Prachaney, and Poungrat Pakdeechote. 2018. "Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression" Nutrients 10, no. 10: 1549. https://doi.org/10.3390/nu10101549

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