CARDIOPROTECTIVE EFFECT OF SEPIA INK AGAINST DOXORUBICIN-INDUCED MYOCARDIAL INFARCTION IN RATS

Introduction: Myocardial infarction (MI) is caused by a reduction or total cessation of blood supply to a section of the myocardium. Despite its potential efficacy in the treatment of various malignancies, doxorubicin’s (DOX) capabilities are limited due to its extensive cardiotoxic effect. Sepia ink (SI) is an alternative medication with numerous therapeutic applications. It possesses anti-oxidant, anti-radiation, and anti-bacterial characteristics. The current study aims to evaluate the protective effect of SI against DOX -induced myocardial infarction in rats. Methods: A total cumulative dose of DOX (18 mg/kg body weight, i.p.) was administrated once daily on days 2, 4, 6, 8, 10, and 12 (i.p.) to induce MI in rats. 18 rats were divided into 3 groups; control, MI, and MI treated with SI (200 mg/kg, orally). Results: Treatment with SI restored theST-segment to near-normal levels. SI decreased levels of cardiac troponin T, creatine kinase, lactate dehydrogenase,aspartate aminotransferase, alkaline phosphatase, alanine amino transferase, malondialdehyde, While it increased nitic oxide, catalase, and reduced glutathione levels. The histological studies found that the SI-treated group demonstrated significant improvement in the heart and liver tissues with reduction in collagen deposition. Discussion: SI demonstrated cardioprotective properties in the myocardial infarcted rats by boosting the antioxidant system and stimulating nitric oxide production. Conclusion: This study showed that SI serve as a promising therapeutic agent for mitigating.

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Publication Details

Journal
Infarma - Ciências Farmacêuticas
Published
2026-11-09
DOI
https://doi.org/10.14450/infarma.e202614
Primary Topic
Chemotherapy-induced cardiotoxicity and mitigation
Type
article
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article

CARDIOPROTECTIVE EFFECT OF SEPIA INK AGAINST DOXORUBICIN-INDUCED MYOCARDIAL INFARCTION IN RATS

Amel M. Soliman, Ayman Saber Mohamed, Mohamed Fahmy Ali Shehata
Infarma - Ciências Farmacêuticas
Chemotherapy-induced cardiotoxicity and mitigation
article

CARDIOPROTECTIVE EFFECT OF SEPIA INK AGAINST DOXORUBICIN-INDUCED MYOCARDIAL INFARCTION IN RATS

Amel M. Soliman, Ayman Saber Mohamed, Mohamed Fahmy Ali Shehata
article en

Abstract

Introduction: Myocardial infarction (MI) is caused by a reduction or total cessation of blood supply to a section of the myocardium. Despite its potential efficacy in the treatment of various malignancies, doxorubicin’s (DOX) capabilities are limited due to its extensive cardiotoxic effect. Sepia ink (SI) is an alternative medication with numerous therapeutic applications. It possesses anti-oxidant, anti-radiation, and anti-bacterial characteristics. The current study aims to evaluate the protective effect of SI against DOX -induced myocardial infarction in rats. Methods: A total cumulative dose of DOX (18 mg/kg body weight, i.p.) was administrated once daily on days 2, 4, 6, 8, 10, and 12 (i.p.) to induce MI in rats. 18 rats were divided into 3 groups; control, MI, and MI treated with SI (200 mg/kg, orally). Results: Treatment with SI restored theST-segment to near-normal levels. SI decreased levels of cardiac troponin T, creatine kinase, lactate dehydrogenase,aspartate aminotransferase, alkaline phosphatase, alanine amino transferase, malondialdehyde, While it increased nitic oxide, catalase, and reduced glutathione levels. The histological studies found that the SI-treated group demonstrated significant improvement in the heart and liver tissues with reduction in collagen deposition. Discussion: SI demonstrated cardioprotective properties in the myocardial infarcted rats by boosting the antioxidant system and stimulating nitric oxide production. Conclusion: This study showed that SI serve as a promising therapeutic agent for mitigating.

Infarma - Ciências FarmacêuticasVol. 38
Chemotherapy-induced cardiotoxicity and mitigation
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CARDIOPROTECTIVE EFFECT OF SEPIA INK AGAINST DOXORUBICIN-INDUCED MYOCARDIAL INFARCTION IN RATS — Amel M. Soliman, Ayman Saber Mohamed, et al. · Infarma - Ciências Farmacêuticas (2026) | TGRS Research Map | TGRS