| Abstract |
Genistein is an isoflavone found in soybeans. This study evaluates the protective effects
of genistein on Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension,
cardiac remodeling, and dysfunction in rats. Male Wistar rats were treated with L-NAME 40
mg/kg/day together for 5 weeks, with or without genistein at a dose of 40 or 80 mg/kg/day or lisinopril 5 mg/kg/day (n = 8 per group). Genistein prevented L-NAME-induced hypertension in rats.
Increases in the left ventricular weight, metalloproteinase-2, metalloproteinase-9, and collagen type
I intensity were observed in L-NAME rats, and these changes were attenuated in the genisteintreated group. Genistein reduced circulating angiotensin-converting enzyme activity and angiotensin II concentrations in L-NAME rats. L-NAME increased plasma and cardiac malondialdehyde and
vascular superoxide generations, as well as reductions of serum and cardiac catalase activities in
rats. Plasma nitrate/nitrite were protected in the genistein-treated group. Genistein prevented the
L-NAME-induced overexpression of angiotensin II receptor type I (AT1R), nicotinamide adenine
dinucleotide phosphate (NADPH) oxidase subunit 2 (gp91phox), and transforming growth factor
beta I (TGF-β1) in hypertensive rats. In conclusion, genistein exhibited a cardioprotective effect in
hypertensive rats in this study. The molecular mechanisms might be mediated by suppression of
oxidative stress through the Ang II/AT1R/NADPH oxidase/TGF-β1 signaling pathway. |
Publication
Journal Publication
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