| Abstract |
Genistein is a bioflavonoid mainly found in soybean. This study evaluated the effect of genistein on vascular
dysfunction and kidney damage in two-kidney, one-clipped (2K1C) hypertensive rats. Male Sprague–Dawley2K1C hypertensive rats were treated with genistein (40 or 80 mg/kg) or losartan 10 mg/kg (n = 8/group).
Genistein reduced blood pressure, attenuated the increase in sympathetic nerve-mediated contractile response
and endothelial dysfunction in the mesenteric vascular beds and aorta of 2K1C rats. Increases in the intensity of
tyrosine hydroxylase (TH) in the mesentery and plasma norepinephrine (NE) were alleviated in the genisteintreated group. Genistein also improved renal dysfunction, hypertrophy of the non-clipped kidney (NCK) and
atrophy of the clipped kidney (CK) in 2K1C rats. Upregulation of angiotensin II receptor type I (AT1R), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit 4 (Nox4) and Bcl2-associated X protein
(BAX) and downregulation of B-cell lymphoma 2 (Bcl2) protein found in CK were restored by genistein. It also
suppressed the overexpression of AT1R, transforming growth factor beta I (TGF-β1), smad2/3 and p-smad3 in
NCK. Genistein reduced serum angiotensin converting enzyme (ACE) activity and plasma angiotensin II (Ang II)
in 2K1C rats. Low levels of catalase activity as well as high levels of superoxide generation and malondialdehyde
(MDA) in 2K1C rats were restored by genistein treatment. In conclusion, genistein suppressed renin-angiotensin
system-mediated sympathetic activation and oxidative stress in 2K1C rats. It alleviated renal atrophy in CK via
modulation of AT1R/NADPH oxidase/Bcl-2/BAX pathways and hypertrophy in NCK via AT1R/TGF-β1/smad-dependent signalling pathways |
Publication
Journal Publication
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