2012 ©
             Publication
Journal Publication
Title of Article Genistein alleviates renin-angiotensin system mediated vascular and kidney alterations in renovascular hypertensive rats 
Date of Acceptance 25 December 2021 
Journal
     Title of Journal Biomedicine & Pharmacotherapy 
     Standard SCOPUS 
     Institute of Journal Elsevier Masson SAS 
     ISBN/ISSN  
     Volume  
     Issue 146 
     Month February
     Year of Publication 2022 
     Page  
     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 
     Keyword Genistein Renin angiotensin system Oxidative stress Vascular dysfunction Kidney damage Renovascular hypertension 
Author
627070017-7 Mr. ANUSON POASAKATE [Main Author]
Medicine Doctoral Degree

Reviewing Status มีผู้ประเมินอิสระ 
Status ตีพิมพ์แล้ว 
Level of Publication นานาชาติ 
citation true 
Part of thesis true 
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