CARDIOPROTECTIVE EFFECT OF CO-ENZYME Q10 ON DOXORUBICIN INDUCED CARDIOTOXICITY IN ADULT MALE ALBINO WISTAR RAT

Physiology 2023 (Harrogate, UK) (2023) Proc Physiol Soc 54, PCB017

Poster Communications: CARDIOPROTECTIVE EFFECT OF CO-ENZYME Q10 ON DOXORUBICIN INDUCED CARDIOTOXICITY IN ADULT MALE ALBINO WISTAR RAT

Enivwenaye Nabofa1, EKEMINIMFON-ABASI EMMANUEL Okon1,

1Babcock University Ilishan-Remo Nigeria,

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Introduction: Doxorubicin (DOX) is a widely used chemotherapeutic agent but it is limited by its cardio-toxic side effect. Coenzyme Q10 (CoQ10) which could be considered as a vitamin is one of the most significant lipid antioxidants, which prevents the generation of free radicals and modifications of proteins, lipids, and DNA. However, it is not known whether CoQ10 is capable of preventing or ameliorating DOX induced cardiotoxicity.

Aim: The present study was thus designed to ascertain the cardioprotective effects of CoQ10 on DOX induced cardiotoxicity.

Method: All procedures were undertaken in accordance with regulations as set out by the Babcock University Research and Ethical Committee (BUREC). Adult male Wister rats weighing 180-200 g were randomly divided into five groups (n=7). Animal experimentation lasted for 14 days. Group 1 animals served as control and were untreated. Groups 3-5 animals were treated with dexamethasone (3 mg/Kg), CoQ10 (1 and 10 mg/kg) respectively, for 14 days. Group 2-5 animals were given a single dose of DOXO (15 mg/Kg) on day 11 of the study. Cardiovascular, biochemical, histological and molecular parameters were determined at the end of the study.

Results: DOXO altered cardiovascular function in rats evidenced by cardiac arrhythmia, hyperlipidemia and increased serum creatine kinase-myocardial band (CK-MB) levels which was associated with increased cardiac oxidative stress markers. CoQ10 especially at the higher dose ameliorated the DOXO induced cardiovascular dysfunction which was associated with decrease cardiac expressions of TNF-α and GSK3B genes.

Conclusion:  CoQ10 especially at 10 mg/Kg mitigated DOXO induced cardiac dysfunction which involved the modulation of TNF-α / GSK3B signaling pathway.



Where applicable, experiments conform with Society ethical requirements.

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