Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice

Abstract Background The toxic effect of doxorubicin on the heart limits its clinical usage in cancer therapy. This work intended to investigate, for the first time, the efficacy of rifampicin administration against doxorubicin-induction of cardiotoxicity in mice. Forty adult male albino mice were di...

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Main Authors: Omnia A. Basal, Rasha F. Zahran, Entsar A. Saad
Format: Article
Language:English
Published: SpringerOpen 2023-08-01
Series:The Egyptian Heart Journal
Subjects:
Online Access:https://doi.org/10.1186/s43044-023-00403-z
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author Omnia A. Basal
Rasha F. Zahran
Entsar A. Saad
author_facet Omnia A. Basal
Rasha F. Zahran
Entsar A. Saad
author_sort Omnia A. Basal
collection DOAJ
description Abstract Background The toxic effect of doxorubicin on the heart limits its clinical usage in cancer therapy. This work intended to investigate, for the first time, the efficacy of rifampicin administration against doxorubicin-induction of cardiotoxicity in mice. Forty adult male albino mice were distributed into four sets: Control, Doxorubicin, Doxorubicin + Rifampicin 0.107, and Doxorubicin + Rifampicin 0.214, with n = 10 for each. Heart histopathology and biochemical assays for heart function tests [creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), cardiac troponin I (cTnI), atrial natriuretic peptide (ANP), and vascular endothelial growth factor (VEGF)], oxidative stress [malondialdehyde (MDA) and superoxide dismutase (SOD)], and minerals [phosphorus, sodium, potassium, and calcium] were done. Results Doxorubicin-induced cardiotoxicity using a total dose of 15 mg/kg was confirmed histologically. Cardiomyocytes showed congestion, necrosis, edema, and inflammatory cell infiltration. Biochemically, elevations in LDH, CK, and AST activities, p < 0.001, as well as increases in cTnI and ANP levels, p < 0.001, increased oxidative stress (MDA, p < 0.001), high minerals (Na, K, p < 0.001, P, p < 0.01, and Ca, p < 0.05), with reduced VEGF concentration, p < 0.001, and low antioxidant (SOD, p < 0.001) were observed in the Doxorubicin group compared to control. Co-treatment with rifampicin significantly (p < 0.001) reduced the increased oxidative stress, high Na and K, increased LDH, CK, AST, cTnI, and ANP, and elevated the low SOD toward the normal ranges. Our histological data supported our biochemical data; rifampicin dose 0.214 mg/kg showed better improvements than dose 0107. Conclusions Our results demonstrated that rifampicin could help protect the body against doxorubicin-induced cardiotoxicity through its antioxidative effect.
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spelling doaj.art-9e94f5bfb8804a1bb9cbc0cb77af201b2023-11-20T09:50:06ZengSpringerOpenThe Egyptian Heart Journal2090-911X2023-08-0175111310.1186/s43044-023-00403-zRifampicin efficacy against doxorubicin-induced cardiotoxicity in miceOmnia A. Basal0Rasha F. Zahran1Entsar A. Saad2Chemistry Department, Faculty of Science, Damietta UniversityChemistry Department, Faculty of Science, Damietta UniversityChemistry Department, Faculty of Science, Damietta UniversityAbstract Background The toxic effect of doxorubicin on the heart limits its clinical usage in cancer therapy. This work intended to investigate, for the first time, the efficacy of rifampicin administration against doxorubicin-induction of cardiotoxicity in mice. Forty adult male albino mice were distributed into four sets: Control, Doxorubicin, Doxorubicin + Rifampicin 0.107, and Doxorubicin + Rifampicin 0.214, with n = 10 for each. Heart histopathology and biochemical assays for heart function tests [creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), cardiac troponin I (cTnI), atrial natriuretic peptide (ANP), and vascular endothelial growth factor (VEGF)], oxidative stress [malondialdehyde (MDA) and superoxide dismutase (SOD)], and minerals [phosphorus, sodium, potassium, and calcium] were done. Results Doxorubicin-induced cardiotoxicity using a total dose of 15 mg/kg was confirmed histologically. Cardiomyocytes showed congestion, necrosis, edema, and inflammatory cell infiltration. Biochemically, elevations in LDH, CK, and AST activities, p < 0.001, as well as increases in cTnI and ANP levels, p < 0.001, increased oxidative stress (MDA, p < 0.001), high minerals (Na, K, p < 0.001, P, p < 0.01, and Ca, p < 0.05), with reduced VEGF concentration, p < 0.001, and low antioxidant (SOD, p < 0.001) were observed in the Doxorubicin group compared to control. Co-treatment with rifampicin significantly (p < 0.001) reduced the increased oxidative stress, high Na and K, increased LDH, CK, AST, cTnI, and ANP, and elevated the low SOD toward the normal ranges. Our histological data supported our biochemical data; rifampicin dose 0.214 mg/kg showed better improvements than dose 0107. Conclusions Our results demonstrated that rifampicin could help protect the body against doxorubicin-induced cardiotoxicity through its antioxidative effect.https://doi.org/10.1186/s43044-023-00403-zAtrial natriuretic peptideCardiac troponinHistopathologyMineralsOxidative stressVascular endothelial growth factor
spellingShingle Omnia A. Basal
Rasha F. Zahran
Entsar A. Saad
Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice
The Egyptian Heart Journal
Atrial natriuretic peptide
Cardiac troponin
Histopathology
Minerals
Oxidative stress
Vascular endothelial growth factor
title Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice
title_full Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice
title_fullStr Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice
title_full_unstemmed Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice
title_short Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice
title_sort rifampicin efficacy against doxorubicin induced cardiotoxicity in mice
topic Atrial natriuretic peptide
Cardiac troponin
Histopathology
Minerals
Oxidative stress
Vascular endothelial growth factor
url https://doi.org/10.1186/s43044-023-00403-z
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AT rashafzahran rifampicinefficacyagainstdoxorubicininducedcardiotoxicityinmice
AT entsarasaad rifampicinefficacyagainstdoxorubicininducedcardiotoxicityinmice