Apremilast prevent doxorubicin-induced apoptosis and inflammation in heart through inhibition of oxidative stress mediated activation of NF-κB signaling pathways.
Pharmacol Rep
; 70(5): 993-1000, 2018 Oct.
Article
en En
| MEDLINE
| ID: mdl-30118964
ABSTRACT
BACKGROUND:
Doxorubicin is an effective, potent and commonly used anthracycline-related anticancer drug; however, cardiotoxicity compromises its therapeutic potential. Apremilast, a novel phosphodiesterase type 4-inhibitor, reported to have anti-inflammatory effects and modulating many inflammatory mediators.METHODS:
The present study investigated the influence of apremilast against doxorubicin-induced cardiotoxicity in male Wistar rats. A total, 24 animals were divided into four groups of six animal each. Group 1, served as control and received normal saline. Group 2 animals, received doxorubicin (20mgkg-1, ip). Group 3 and 4, treatment group, received doxorubicin (20mgkg-1, ip) with the same schedule as group-2, plus apremilast (10 and 20mgkg-1day-1, po) respectively. Oxidative stress, caspase-3 enzyme activity, gene expression and protein expression were tested.RESULTS:
The results of the present study demonstrated that administration of apremilast reversed doxorubicin-induced cardiotoxicity.CONCLUSION:
These findings suggested that apremilast can attenuate doxorubicin-induced cardiotoxicity via inhibition of oxidative stress mediated activation of nuclear factor-kappa B signaling pathways.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Talidomida
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Transducción de Señal
/
Doxorrubicina
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FN-kappa B
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Apoptosis
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Estrés Oxidativo
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Inflamación
Límite:
Animals
Idioma:
En
Revista:
Pharmacol Rep
Asunto de la revista:
FARMACOLOGIA
Año:
2018
Tipo del documento:
Article