Naringenin inhibits N G -nitro-L-arginine methyl ester-induced hypertensive left ventricular hypertrophy by decreasing angiotensin-converting enzyme 1 expression.

Naringenin (NGN) is a natural flavonoid that exerts antiinflammatory, antioxidant and cardioprotective effects. The present study investigated the effects of NGN on left ventricular hypertrophy in rats with NG -nitro-L-arginine methyl ester (L-NAME)-induced hypertension, and sought to determine the underlying mechanism of action. The rats received the following by gavage daily for 56 days: L-NAME (50 mg/kg/day) + NGN (100 mg/kg/day), L-NAME (50 mg/kg/day) + saline, or saline + saline. Blood pressure, heart rate and body weight were recorded. Left ventricular hypertrophy was assessed by echocardiography and hematoxylin-eosin staining. Angiotensin II (Ang II) and angiotensin-converting enzyme 1 (ACE1), which serve a pivotal role in cardiac remodeling, were evaluated by ELISA, reverse transcription-quantitative polymerase chain reaction and western blot analysis. NGN had no significant effect on body weight, heart rate or blood pressure. The extent of left ventricular hypertrophy in the L-NAME + NGN group was lower than in the L-NAME + saline group on day 56. NGN decreased Ang II and ACE1 protein levels in myocardial tissues. In conclusion, Ang II and ACE1 expression in cardiac tissue was inhibited by NGN in L-NAME-treated rats, which may contribute to the inhibitory effects of NGN on left ventricular hypertrophy that is induced by pressure overload.