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.