Pulmonary hypertension is characterized by increased vascular resistances, that could lead to right heart failure and death. Endothelin-1 (ET-1) is a peptide with strong vasoconstrictive and pro-fibrotic properties and is one of the main mediators of pulmonary hypertension. Aminaftone, a synthetic molecule derivative of 4-amynobenzoic acid, down-regulates ET-1 production in vitro by interfering with the transcription of the pre-pro-ET-1 gene. The aim of this study was to test whether the inhibition of ET-1 production by aminaftone attenuates the effects of pulmonary hypertension. Pulmonary hypertension was induced through s.c. injection of 60 mg/kg monocrotaline. The rats were randomly assigned to the following experimental groups: Control; Monocrotaline; Aminaftone 30 mg/kg/day; Aminaftone 150 mg/kg/day. After 5 weeks, mortality was significantly lower in the animals treated with aminaftone at both doses compared to monocrotaline alone. Aminaftone reduced plasma concentration of ET-1 and seemed to reduce right heart hypertrophy and the wall thickness of the pulmonary arteries at the highest dose. Aminaftone may represent a novel treatment strategy of pulmonary hypertension. © 2011 Elsevier B.V. All rights reserved.

Zambelli, V., Santaniello, A., Fumagalli, F., Masson, S., Scorza, R., Beretta, L., et al. (2011). Efficacy of aminaftone in a rat model of monocrotaline-induced pulmonary hypertension. EUROPEAN JOURNAL OF PHARMACOLOGY, 667(1-3), 287-291 [10.1016/j.ejphar.2011.05.060].

Efficacy of aminaftone in a rat model of monocrotaline-induced pulmonary hypertension

ZAMBELLI, VANESSA;
2011

Abstract

Pulmonary hypertension is characterized by increased vascular resistances, that could lead to right heart failure and death. Endothelin-1 (ET-1) is a peptide with strong vasoconstrictive and pro-fibrotic properties and is one of the main mediators of pulmonary hypertension. Aminaftone, a synthetic molecule derivative of 4-amynobenzoic acid, down-regulates ET-1 production in vitro by interfering with the transcription of the pre-pro-ET-1 gene. The aim of this study was to test whether the inhibition of ET-1 production by aminaftone attenuates the effects of pulmonary hypertension. Pulmonary hypertension was induced through s.c. injection of 60 mg/kg monocrotaline. The rats were randomly assigned to the following experimental groups: Control; Monocrotaline; Aminaftone 30 mg/kg/day; Aminaftone 150 mg/kg/day. After 5 weeks, mortality was significantly lower in the animals treated with aminaftone at both doses compared to monocrotaline alone. Aminaftone reduced plasma concentration of ET-1 and seemed to reduce right heart hypertrophy and the wall thickness of the pulmonary arteries at the highest dose. Aminaftone may represent a novel treatment strategy of pulmonary hypertension. © 2011 Elsevier B.V. All rights reserved.
Articolo in rivista - Articolo scientifico
Pulmonary hypertension, Monocrotaline, Aminaftone, Endothelin-1
English
2011
667
1-3
287
291
none
Zambelli, V., Santaniello, A., Fumagalli, F., Masson, S., Scorza, R., Beretta, L., et al. (2011). Efficacy of aminaftone in a rat model of monocrotaline-induced pulmonary hypertension. EUROPEAN JOURNAL OF PHARMACOLOGY, 667(1-3), 287-291 [10.1016/j.ejphar.2011.05.060].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/51477
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