Protective effect of taurine against doxorubicin-induced cardiotoxicity in rats: echocardiographical and histological findings

Barış, Veysel Özgür; Gedikli, Esra; Yersal, Nilgün; Müftüoğlu, Sevda; Erdem, Ayşen

doi:10.1007/s00726-019-02801-7

Cited by 20 publications

(7 citation statements)

References 26 publications

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“…117 While repeated lower doxorubicin intraperitoneal injections (2–3.4 mg/kg doxorubicin) resulted in cardiomyopathy. 118 A cumulative dose of 3 to 25 mg/kg is usually used in the long-term animal model at 1 to 5 mg/kg every week. 119 A short-term, high-dose injection model would be appropriate for assessing acute cardiotoxicity, whereas a long-term, low-dose model would be appropriate for assessing chronic cardiotoxicity.…”

Section: Small Animal Drug-induced Modelsmentioning

confidence: 99%

Large and Small Animal Models of Heart Failure With Reduced Ejection Fraction

Pilz

Chang

Kiss

et al. 2022

Circulation Research

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Heart failure (HF) describes a heterogenous complex spectrum of pathological conditions that results in structural and functional remodeling leading to subsequent impairment of cardiac function, including either systolic dysfunction, diastolic dysfunction, or both. Several factors chronically lead to HF, including cardiac volume and pressure overload that may result from hypertension, valvular lesions, acute, or chronic ischemic injuries. Major forms of HF include hypertrophic, dilated, and restrictive cardiomyopathy. The severity of cardiomyopathy can be impacted by other comorbidities such as diabetes or obesity and external stress factors. Age is another major contributor, and the number of patients with HF is rising worldwide in part due to an increase in the aged population. HF can occur with reduced ejection fraction (HF with reduced ejection fraction), that is, the overall cardiac function is compromised, and typically the left ventricular ejection fraction is lower than 40%. In some cases of HF, the ejection fraction is preserved (HF with preserved ejection fraction). Animal models play a critical role in facilitating the understanding of molecular mechanisms of how hearts fail. This review aims to summarize and describe the strengths, limitations, and outcomes of both small and large animal models of HF with reduced ejection fraction that are currently used in basic and translational research. The driving defect is a failure of the heart to adequately supply the tissues with blood due to impaired filling or pumping. An accurate model of HF with reduced ejection fraction would encompass the symptoms (fatigue, dyspnea, exercise intolerance, and edema) along with the pathology (collagen fibrosis, ventricular hypertrophy) and ultimately exhibit a decrease in cardiac output. Although countless experimental studies have been published, no model completely recapitulates the full human disease. Therefore, it is critical to evaluate the strength and weakness of each animal model to allow better selection of what animal models to use to address the scientific question proposed.

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Section: Small Animal Drug-induced Modelsmentioning

confidence: 99%

Large and Small Animal Models of Heart Failure With Reduced Ejection Fraction

Pilz

Chang

Kiss

et al. 2022

Circulation Research

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“…In short-term rat models animals receive a single dose of DOX (10–30 mg/kg) intravenously ( Todorova et al, 2012 ). Other short-term models use 2–3.4 mg/kg of DOX every other day, six times intraperitoneally (the total dose is 12–20 mg/kg) ( Zbinden et al, 1978 ; Lanza et al, 1989 ; Carvalho et al, 2010 ; Razmaraii et al, 2016 ; Cappetta et al, 2018 ; Aygun and Gul, 2019 ; Barış et al, 2019 ). Long-term rat models typically use 1–5 mg/kg every week for 2–12 weeks with a cumulative dose of 3–25 mg/kg ( Villani et al, 1991 ; Sacco et al, 2001 ; Sayed-Ahmed et al, 2001 ; Rahimi Balaei et al, 2010 ; Hydock et al, 2012 ; Hole et al, 2013 ; Toblli et al, 2014 ; Kang et al, 2017 ; Medeiros-Lima et al, 2019 ; Wang et al, 2019 ; Chakouri et al, 2020 ; Sharma et al, 2020 ).…”

Section: Anthracycline Cardiomyopathy Modelsmentioning

confidence: 99%

Analysis of Models of Doxorubicin-Induced Cardiomyopathy in Rats and Mice. A Modern View From the Perspective of the Pathophysiologist and the Clinician

et al. 2021

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Today the pharmacological possibilities of treating cancer are expanding and as a result, life expectancy is increasing against the background of chemotherapy and supportive treatment. In the conditions of successful antitumor treatment, complications associated with its toxic effect on healthy tissues and organs began to come to the fore. Anthracycline cardiomyopathy was the first serious cardiovascular complication to draw the attention of oncologists and cardiologists around the world. Anthracycline drugs such as doxorubicin, epirubicin, idarubicin are still widely used in oncological practice to treat a wide range of solid and hematological malignancies. Doxorubicin-induced cardiomyopathy is closely associated with an increase in oxidative stress, as evidenced by reactive oxygen species (ROS) nduced damage such as lipid peroxidation, and decreased levels of antioxidants. Myofibrillar destruction and dysregulation of intracellular calcium are also important mechanisms, usually associated with doxorubicin-induced cardiotoxicity. Despite the abundance of data on various mechanisms involved in the implementation of doxorubicin-induced cardiotoxicity, a final understanding of the mechanism of the development of doxorubicin cardiomyopathy has not yet been formed. It poses the most significant challenges to the development of new methods of prevention and treatment, as well as to the unambiguous choice of a specific treatment regimen using the existing pharmacological tools. In order to resolve these issues new models that could reflect the development of the chemotherapy drugs effects are needed. In this review we have summarized and analyzed information on the main existing models of doxorubicin cardiomyopathy using small laboratory animals. In addition, this paper discusses further areas of research devoted to the development and validation of new improved models of doxorubicin cardiomyopathy suitable both for studying the mechanisms of its implementation and for the preclinical drugs effectiveness assessment.

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“…[25] Prior researchs have administered many adjuvants, including amino acids, vitamins, and hormones, to inhibit or lessen the adverse effects of cancer-directed treatments. [26,27] Se has antioxidant and anti-inflammatory impacts and plays a vital role in the cellular antioxidant defense system. [28] It has powerful anticancer properties and has been verified to be an essential trace element for animals and humans, which is critical for the normal function of the body's various systems.…”

Section: Discussionmentioning

confidence: 99%

Studies on the ameliorative potential of dietary supplemented different dose of selenium on doxorubicin‐induced ovarian damage in rat

Cengiz Mat,

Alisan Suna,

Baran

et al. 2023

J Biochem & Molecular Tox

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Doxorubicin (Dox) may induce loss of follicles, resulting in the depletion of ovarian reserve and consequent premature ovarian failure. Selenium (Se) is an oligoelement with fundamental biological features and is among the most common chemical inhibitor compounds. The present study describes the curative effects of dietary supplementation with different Se doses on Dox‐induced ovarian damage in rats. In this study, 64 adult female Wistar rats were randomly separated into eight groups: Control group, Dox group (5 mg/kg intraperitoneal [i.p.]), low‐dose Se (0.5 mg/kg i.p.), middle dose Se (1 mg/kg i.p.), high dose (Se 2 mg/kg i.p.), Dox + low‐dose Se group (0.5 mg/kg i.p.), Dox + middle dose Se (1 mg/kg i.p.), and Dox + high‐dose Se group (2 mg/kg i.p.). After the experiment, ovarian follicles were counted, and Antimüllerian hormone, interleukin 1 beta, tumor necrosis factor alpha, and caspase‐3 expression were determined. Levels of malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase were biochemically measured in ovarian tissue. Dox caused ovarian injury, as evidenced by significant changes in ovarian markers, histological abnormalities, and the debilitation of antioxidant defense mechanisms. Furthermore, Dox therapy significantly changed the expression of inflammatory and apoptotic markers. Dox + 1 mg Se with various saturations was studied, and this study demonstrated both histopathological and follicular reserve and more protective features. 1 mg Se pretreatment improved Dox‐induced ovarian toxicity through alleviating the antioxidant mechanism, decreasing inflammation and apoptosis, and restoring ovarian architecture. As a result, our findings indicate that 1 mg Se is a promising therapeutic agent for the prevention of ovarian damage associated with Dox.

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Protective effect of taurine against doxorubicin-induced cardiotoxicity in rats: echocardiographical and histological findings

Cited by 20 publications

References 26 publications

Large and Small Animal Models of Heart Failure With Reduced Ejection Fraction

Large and Small Animal Models of Heart Failure With Reduced Ejection Fraction

Analysis of Models of Doxorubicin-Induced Cardiomyopathy in Rats and Mice. A Modern View From the Perspective of the Pathophysiologist and the Clinician

Studies on the ameliorative potential of dietary supplemented different dose of selenium on doxorubicin‐induced ovarian damage in rat

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