Doxorubicin-Induced Cardiomyopathy in Rats: Behavior of the Animals in the Open Field

Rodynskii, O. G.; Кozlova, Yu. V.; Козлов, С. В.; Rodynska, G. O.; Sapozhnychenko, L. V.

doi:10.1007/s11062-018-9747-x

Cited by 3 publications

(1 citation statement)

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“…Unfortunately, treatment for established cardiomyopathy induced by doxorubicin has no effective treatment presently available (Chatterjee et al, 2010;dos Santos and dos Santos Goldenberg, 2018). Many reported doxorubicin to cause cardiomyopathy in-vivo in different animal species (Chen et al, 2015;O'Connell et al, 2017;Rodynskii et al, 2018) and also confirmed induction cardiotoxicity and oxidative stress in experimental models by doxorubicin. In cardiac tissue, a toxic and short-lived converted metabolite of doxorubicin that is its semiquinone form interacts with molecular oxygen and initiates a prominent role of ROS generation cascade including hydroxyl radical production in doxorubicin-induced cardiotoxicity (Asensio-L opez et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Nrf2 by quercetin in doxorubicin-treated rats

Sharma

Parikh

Shah

et al. 2020

Heliyon

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Doxorubicin (DOXO), a potent and widely used chemotherapeutic agent, causes irreversible heart failure by increasing oxidative stress, which limits its clinical utility. Nuclear factor erythroid-derived 2 -like 2 (Nrf2) is a prominent central regulator of cellular impenetrable to oxidants. The purpose of the study is to assess the ameliorative outcome of quercetin in cardiomyopathic rats induced by doxorubicin. Cardiomyopathy was produced in rats by single intraperitoneal weekly with DOXO (2 mg/kg) for 4 weeks. The rats were divided into five groups: (I) control group; (II) DOXO (2 mg/kg, i.p.) group; (III-V) DOXO þ quercetin (10 mg/kg, 25 mg/kg and 50 mg/kg, orally), and were treated for 7 weeks. At the end of the treatment duration, cardiac function and biochemical parameters were assessed. Quercetin (10 mg/kg, 25 mg/kg and 50 mg/kg, orally) treatment reduced the raised blood pressure (BP) and left ventricular dysfunction. Withal, it prevented the rise in CKMB and LDH, suggesting the effect of quercetin in the maintaining the integrity of the cell membrane Besides, it also prevented the alteration in electrolyte levels, the activity of ATPase, and antioxidant status. Quercetin increased Nrf2 mRNA expression and reduced histological abnormalities compared 1 to the DOXO control group. In conclusion, quercetin protected against DOXO-induced cardiomyopathy, by increasing expression of NRF2, and thereby increasing antioxidant defense and restoring biochemical and histological abnormalities.

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