Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity

Doxorubicin belongs to the class of anthracycline antibiotics that is widely used in the treatment protocols of a wide range of malignancies. The major deleterious effect of doxorubicin use is the possible occurrence of cardiotoxicity. This study aimed to delineate the possible effects of targeting...

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Autores principales:	Ahmed M. Kabel, Samir A. Salama, Almokhtar A. Adwas, Remon S. Estfanous
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	fraxetin doxorubicin cardiotoxicity oxidative stress autophagy rats Medicine R Pharmacy and materia medica RS1-441
Acceso en línea:	https://doaj.org/article/67c1e10e5a264df29bd87b4550ef4ecc
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spelling	oai:doaj.org-article:67c1e10e5a264df29bd87b4550ef4ecc2021-11-25T18:40:03ZTargeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity10.3390/ph141111881424-8247https://doaj.org/article/67c1e10e5a264df29bd87b4550ef4ecc2021-11-01T00:00:00Zhttps://www.mdpi.com/1424-8247/14/11/1188https://doaj.org/toc/1424-8247Doxorubicin belongs to the class of anthracycline antibiotics that is widely used in the treatment protocols of a wide range of malignancies. The major deleterious effect of doxorubicin use is the possible occurrence of cardiotoxicity. This study aimed to delineate the possible effects of targeting oxidative stress, NLRP3 inflammasome, and autophagy by fraxetin on doxorubicin-induced cardiac dysfunction in rats. In a model of doxorubicin-induced cardiotoxicity, the effects of different doses of fraxetin were assessed by determination of biochemical, histopathological, immunohistochemical, and electron microscopic changes. Fraxetin, in a dose-dependent manner, was found to have the ability to mitigate the harmful effects of oxidative stress and inflammation on myocardial muscles with significant decrease in NLRP3 inflammasome, augmentation of autophagy, and amelioration of the apoptotic signaling pathways. In addition, fraxetin, in a dose-dependent manner, had the ability to combat the echocardiographic, histopathological, immunohistochemical, and electron microscopic changes induced by doxorubicin in cardiomyocytes. As a result, fraxetin may be put into consideration as a new adjuvant line of therapy on the way to mitigate doxorubicin-induced cardiotoxicity.Ahmed M. KabelSamir A. SalamaAlmokhtar A. AdwasRemon S. EstfanousMDPI AGarticlefraxetindoxorubicincardiotoxicityoxidative stressautophagyratsMedicineRPharmacy and materia medicaRS1-441ENPharmaceuticals, Vol 14, Iss 1188, p 1188 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	fraxetin doxorubicin cardiotoxicity oxidative stress autophagy rats Medicine R Pharmacy and materia medica RS1-441
spellingShingle	fraxetin doxorubicin cardiotoxicity oxidative stress autophagy rats Medicine R Pharmacy and materia medica RS1-441 Ahmed M. Kabel Samir A. Salama Almokhtar A. Adwas Remon S. Estfanous Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity
description	Doxorubicin belongs to the class of anthracycline antibiotics that is widely used in the treatment protocols of a wide range of malignancies. The major deleterious effect of doxorubicin use is the possible occurrence of cardiotoxicity. This study aimed to delineate the possible effects of targeting oxidative stress, NLRP3 inflammasome, and autophagy by fraxetin on doxorubicin-induced cardiac dysfunction in rats. In a model of doxorubicin-induced cardiotoxicity, the effects of different doses of fraxetin were assessed by determination of biochemical, histopathological, immunohistochemical, and electron microscopic changes. Fraxetin, in a dose-dependent manner, was found to have the ability to mitigate the harmful effects of oxidative stress and inflammation on myocardial muscles with significant decrease in NLRP3 inflammasome, augmentation of autophagy, and amelioration of the apoptotic signaling pathways. In addition, fraxetin, in a dose-dependent manner, had the ability to combat the echocardiographic, histopathological, immunohistochemical, and electron microscopic changes induced by doxorubicin in cardiomyocytes. As a result, fraxetin may be put into consideration as a new adjuvant line of therapy on the way to mitigate doxorubicin-induced cardiotoxicity.
format	article
author	Ahmed M. Kabel Samir A. Salama Almokhtar A. Adwas Remon S. Estfanous
author_facet	Ahmed M. Kabel Samir A. Salama Almokhtar A. Adwas Remon S. Estfanous
author_sort	Ahmed M. Kabel
title	Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity
title_short	Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity
title_full	Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity
title_fullStr	Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity
title_full_unstemmed	Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity
title_sort	targeting oxidative stress, nlrp3 inflammasome, and autophagy by fraxetin to combat doxorubicin-induced cardiotoxicity
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/67c1e10e5a264df29bd87b4550ef4ecc
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Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity

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