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 genistein-treated 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.
Highlights
Hypertension is a chronic disease and a major cause of organ damage and other related diseases, such as coronary artery disease, stroke, kidney disease, heart failure, etc
Oral administration with genistein or in L-NAME-treated rats significantly prevented the development of systolic blood pressure (SP) compared to unlisinopril in L-NAME-treated rats significantly prevented the development of SP compared treated hypertensive ratshypertensive (p < 0.05)
Abnormal remodeling of the Left ventricular (LV) collagen matrix is a major cause of an impairment in terms of cardiac contractility [59], and the present study found reductions of stroke volume (SV), ejection fraction (EF), and fraction shortening (FS) in L-NAME rats
Summary
Hypertension is a chronic disease and a major cause of organ damage and other related diseases, such as coronary artery disease, stroke, kidney disease, heart failure, etc. Chronic hypertension without optimal blood pressure (BP) control can cause cardiac hypertrophy and remodeling, which progressively develops to the impairment of cardiac contractility [1,2]. Production in rats has resulted in high BP, cardiac hypertrophy, and remodeling [5,6]. Bunbupha and coworkers demonstrated that L-NAME hypertensive rats have low plasma NO levels, hypertension, LV hypertrophy, and LV fibrosis [7]. The impairment of LV function has been demonstrated in rats that have received L-NAME, supported by a reduced maximum +LVdP/dt and minimum −LVdP/dt, ejection fraction (EF), stroke volume (SV), and fraction shortening (FS) [8,9]. There is substantial evidence to support the pathological process of cardiac remodeling associated with the renin–angiotensin system
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