Quercetin augments the protective effect of losartan against chronic doxorubicin cardiotoxicity in rats

Matouk, Asmaa I.; Taye, Ashraf; Heeba, Gehan H.; El‐Moselhy, Mohamed A.

doi:10.1016/j.etap.2013.05.006

Cited by 64 publications

(54 citation statements)

References 42 publications

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“…It suggested that the biochemical anomalies might lead to cardiotoxicity. These present observations corroborated to the earlier experimental reports (Koti et al, 2013;Mantawy et al, 2014;Matouk et al, 2013;Mukherjee et al, 2003;Singh et al, 2012). Cardiomyocytes are more susceptible to Dox-induced damage than other tissues due to highly active metabolic machinery in heart (Nohl et al, 1998;Zhang et al, 2009).…”

Section: Discussionsupporting

confidence: 83%

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Kwatra

Kumar

Jangra

et al. 2015

Pharmaceutical Biology

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Context: Doxorubicin (Dox) is one of the most active chemotherapeutic agents used to treat various types of cancers. Its clinical utility is compromised due to fatal cardiac toxicity characterized by an irreversible cardiomyopathy. Objective: This study evaluates the cardioprotective potential of naringin (NR) against Dox-induced acute cardiac toxicity in rats. Materials and methods: Male Wistar rats were randomly divided into five groups. NR (50 and 100 mg/kg) was administered intraperitoneally (i.p.) daily from 0 to 14 d. Doxorubicin (15 mg/kg, i.p.) was given as a single dose on the 10th day. On the 14th day, all animals were sacrificed and oxidative stress parameters that include malondialdehyde (MDA), glutathione (GSH) level, superoxide dismutase (SOD), catalase (CAT) activities, and all mitochondrial complexes (I-IV) activities were evaluated along with histopathological studies of the heart. Results: Doxorubicin-induced cardiotoxicity was confirmed by increased (p50.05) MDA, decreased (p50.05) GSH levels, SOD, and CAT activities, mitochondrial complexes (I-IV) activities in the heart tissue. NR (100 mg/kg) showed cardioprotection as evident from significant decreased MDA (p50.001) level, raised (p50.001) GSH level, SOD and CAT activities and increased mitochondrial complexes I (p50.01), II (p50.001), III (p50.001), and IV (p50.05) activities. Further, Dox-induced cardiotoxicity was confirmed by histopathological studies. These obtained results indicated the protective role of NR against Dox-induced cardiac toxicity in rats. Conclusion: NR can be used in combination with Dox due to its high cardioprotective effect against Dox-induced cardiomyopathy.

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Section: Discussionsupporting

confidence: 83%

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Kwatra

Kumar

Jangra

et al. 2015

Pharmaceutical Biology

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“…CAT, MDA, SOD and GSH-Px are important markers of oxidative stress and are widely regarded as indicators of oxidative injury [23, 24]. We measured levels of these markers to test whether pre-treatment with oxymatrine improved doxorubicin-induced metabolic derangements in rat myocardium.…”

Section: Resultsmentioning

confidence: 99%

Oxymatrine Ameliorates Doxorubicin-Induced Cardiotoxicity in Rats

Zhang

Huang

2017

Cell Physiol Biochem

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Background/Aims: Doxorubicin-induced cardiac toxicity has been a major concern of oncologists and is considered the main restriction on its clinical application. Oxymatrine has shown potent anti-cancer, anti-fibrosis, and anti-oxidative effects. Recently, it has been reported that oxymatrine is protective against some cardiovascular diseases. In this study, we aimed to investigate the effects of oxymatrine on doxorubicin-induced cardiotoxicity in rat hearts and H9c2 cells. Methods: Creatine Kinase - MB (CK-MB) and Lactate Dehydrogenase (LDH) levels were determined using commercial kits. Biochemical indices reflecting oxidative stress, such as catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were also analyzed with commercial kits. Mitochondrial reactive oxygen species (ROS) 2’,7’-dichlorofluorescin diacetate (DCFH-DA) was measured by fluorescence microscopy. Histological analyses were conducted to observe morphological changes, and apoptosis was measured using a commercial kit. Western blots were used to detect the level of expression of cleaved caspase-3. Results: Doxorubicin treatment significantly increased oxidative stress levels, as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen species. Doxorubicin also increased pathological damage in myocardial tissue, myocardial ROS levels, and malonyldialdehyde levels, and induced apoptosis in myocardial tissues and H9c2 cells. All of these doxorubicin-induced effects were attenuated by oxymatrine. Conclusion: These in vitro and in vivo findings indicate that oxymatrine may be a promising cardioprotective agent against doxorubicin-induced cardiotoxicity, at least in part mediated through oxymatrine’s inhibition of cardiac apoptosis and oxidative stress.

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“…The central nervous system, possessing relatively weak endogenous and exogenous antioxidant capabilities, is particularly sensitive to oxidative stress induced by the presence of free radicals (Matouk et al 2013). In the present study, we examined markers of oxidative stress and evaluated antioxidant capacity in fetal brain tissues following exposure of the mother to chemotherapeutic agents known to induce oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Effect of chemotherapy exposure prior to pregnancy on fetal brain tissue and the potential protective role of quercetin

et al. 2014

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Cyclophosphamide (CYC) and doxorubicin (DOX) are among the most effective and widely used anticancer chemotherapeutic drugs. Potential chemopreventive and chemotherapeutic functions have recently been attributed to flavonoids. We hypothesized that Quercetin (QR) would protect against the toxic effects of chemotherapeutic agents applied prior to pregnancy. Rats were treated with the chemotherapeutic drugs CYC (27 mg/kg) and DOX (1.8 mg/kg) applied in a single intraperitoneal dose once every 3 weeks for 10 weeks. QR was administered at a dose of 10 mg/kg/day by oral gavage. 48 h following the experimental chemotherapy exposure, female rats were transferred to cages containing male rat for mating. Fetal brain tissues were removed from fetuses extracted by cesarean section on the 20th day of gestation for evaluation of antioxidant parameters. A significant increase in superoxide dismutase and malondialdehyde activity was observed in CYC and DOX treatment groups relative to the control group (p \ 0.05). Similarly, carnitine acylcarnitine translocase and Glutathione activity was significantly reduced in the CYC and DOX groups relative to the control group (p \ 0.05). Our results indicate that the use of chemotherapeutic drugs before pregnancy can result in oxidative damage to fetal brain tissue. Therefore, women who have been exposed to chemotherapy and may become pregnant should be treated with antioxidant compounds such as QR to reduce the risk of damage to fetal brain tissues.

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Quercetin augments the protective effect of losartan against chronic doxorubicin cardiotoxicity in rats

Cited by 64 publications

References 42 publications

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Oxymatrine Ameliorates Doxorubicin-Induced Cardiotoxicity in Rats

Effect of chemotherapy exposure prior to pregnancy on fetal brain tissue and the potential protective role of quercetin

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