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Hesperidin inhibits L‐NAME‐induced vascular and renal alterations in rats by suppressing the renin–angiotensin system, transforming growth factor‐β1, and oxidative stress
Author(s) -
Bunbupha Sarawoot,
Apaijit Kwanjit,
Potue Prapassorn,
Maneesai Putcharawipa,
Pakdeechote Poungrat
Publication year - 2021
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13438
Subject(s) - hesperidin , captopril , endocrinology , medicine , oxidative stress , angiotensin ii , malondialdehyde , chemistry , kidney , renin–angiotensin system , superoxide dismutase , pharmacology , blood pressure , alternative medicine , pathology
The protective effect of hesperidin on vascular and renal alterations and possible underlying mechanisms involved in N ω ‐nitro‐L‐arginine methyl ester hydrochloride (L‐NAME)‐induced hypertensive rats were investigated in this study. Male Sprague‐Dawley rats were administered L‐NAME (40 mg/kg/day), L‐NAME plus hesperidin (30 mg/kg/day), and L‐NAME plus captopril (2.5 mg/kg/day) for 5 weeks. Hesperidin and captopril significantly prevented L‐NAME‐induced hypertension, vascular and renal dysfunction, intrarenal artery remodelling, glomerular extracellular matrix accumulation, and renal fibrosis. The preventive treatment with hesperidin and captopril also significantly decreased serum angiotensin‐converting enzyme activity and plasma transforming growth factor‐β1 (TGF‐β1) levels and downregulated angiotensin II receptor type I and TGF‐β1 protein expression in the kidneys. In addition, decreased malondialdehyde levels and increased superoxide dismutase activity in the plasma and kidney were observed after co‐treatment with hesperidin or captopril. These findings suggest that hesperidin inhibits L‐NAME‐induced vascular and renal alterations in rats. The possible mechanism may be related to the suppression of the activation of the renin–angiotensin system and expression of TGF‐β1, and reduction of oxidative stress.