Epigallocatechin-3-gallate pretreatment attenuates doxorubicin-induced cardiotoxicity in rats: A mechanistic study

Saeed, Noha M.; El-Naga, Reem N.; El-Bakly, Wesam M.; Abdel-Rahman, Hanaa M.; El-Din, Rania A. Salah; El‐Demerdash, Ebtehal

doi:10.1016/j.bcp.2015.02.006

Cited by 92 publications

(53 citation statements)

References 87 publications

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“…Similar biochemical changes have been seen in several other studies (Fouad et al, 2013;Andreadou et al, 2014;Saeed et al, 2015). The elevated levels of MDA and NO, due to the doxorubicin-induced toxicity, were significantly impeded by AcoA treatment.…”

Section: Discussionsupporting

confidence: 71%

“…Importantly, doxorubicin treatment was also shown to evoke the activation of the proinflammatory nuclear factor kB (NF-кB) with subsequent inflammatory reactions, which lead ultimately to cardiomyocyte apoptosis and dysfunction (Nozaki et al, 2004). This finding was supported by several other studies demonstrating the key role of NF-кB activation in doxorubicin-induced cardiomyopathy (Wang et al, 2002;Fouad et al, 2013;Saeed et al, 2015).…”

Section: Introductionmentioning

confidence: 71%

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The Cardenolide Glycoside Acovenoside A Affords Protective Activity in Doxorubicin-Induced Cardiotoxicity in Mice

Ezzat

Gaafary

Sayed

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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The current study aimed to investigate the protective effect of the cardenolide glycoside acovenoside A (AcoA) against doxorubicininduced cardiotoxicity in mice. AcoA was isolated from the pericarps of Acokanthera oppositifolia to chemical homogeneity and characterized by means of one-and two-dimensional nuclear magnetic resonance spectroscopy. AcoA exhibited relatively low toxicity in mice (LD 50 5 223.3 mg/kg bw). Repeated administration of doxorubicin induced cardiotoxicity manifested by reduced activity of myocardial membrane-bound ion pumps and elevated serum biomarkers of myocardial dysfunction, oxidative stress, and inflammation. Pretreatment of doxorubicin-exposed mice with AcoA (11.16 or 22.33 mg/kg bw, i.p.) for 2 weeks after 2 weeks of combined administration of AcoA and doxorubicin protected the animals dose dependently against doxorubicininduced cardiotoxicity as indicated by normalization of the levels of different myocardial markers of oxidative stress (malondialdehyde, nitric oxide, total antioxidant capacity, and cardiac glutathione), serum myocardial diagnostic marker enzymes (serum cardiac troponin T, creatine kinase isoenzyme MB, aspartate aminotransferase, and lactate dehydrogenase), and inflammatory markers (c-reactive protein, tumor necrosis factor-a, and interleukin-6), as well as myocardial Na 1 /K 1 -ATPase activity. These effects were attributed to the negative impact of AcoA on transcription factors nuclear factor kB and interferon regulatory factor 3/7. Thus acovenoside A might act as a cardioprotective agent to prevent doxorubicin-induced cardiotoxicity.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 71%

The Cardenolide Glycoside Acovenoside A Affords Protective Activity in Doxorubicin-Induced Cardiotoxicity in Mice

Ezzat

Gaafary

Sayed

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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“…22,28,42,43 In addition to its direct toxic effects, ROS can induce nuclear transcription factor-kB (NF-kB) activation which leads to its translocation into the nucleus where it binds to the promoter elements and activate the expression of inflammatory cytokine genes with subsequent proinflammatory mediators production such as TNF-a, COX-2, and NO. 7,44 In the current study, DOX administration resulted in the increased expression of NF-kB as well as increased levels of TNF-a and NO. These results are in accordance with previous investigations that reported the ability of DOX to induce potent inflammatory response through activation of NF-kB and stimulating subsequent proinflammatory cytokine production.…”

Section: Discussionmentioning

confidence: 52%

“…4 DOX has been shown to induce the pro-apoptotic activation of nuclear factor-kappa B (NF-kB) in endothelial cells and cardiomyocytes. [5][6][7] This leads to increase in the production of several proinflammatory cytokines such as tumor necrosis factoralpha (TNF-a) and nitric oxide (NO). 8 Administration of agents such as epigallocatechin-3-gallate that interferes with NF-kB signaling pathway has shown significant potential to attenuate DOX-induced cardiac damage.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effects of sitagliptin against doxorubicin-induced cardiotoxicity in rats

El‐Agamy

Abo‐Haded

Elkablawy

2016

Exp Biol Med (Maywood)

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There is a large body of evidence suggesting that inhibitors of dipeptidyl peptidase-4, such as sitagliptin, may exhibit beneficial effects against different inflammatory disorders. This investigation was conducted to elucidate the potential ability of sitagliptin to counteract the injurious effects of doxorubicin in cardiac tissue. Male Wistar rats were pretreated with sitagliptin for 10 days then treated with a single dose of doxorubicin (20 mg/kg, i.p). Electrocardiography, biochemical estimation of serum and tissue markers, and histo-and immunopathological examinations were done. Results have shown that supplementation with sitagliptin resulted in significant improvement of cardiac function with contaminant decrease in serum markers of doxorubicin-induced cardiotoxicity. These results were supported by the histopathological results. Furthermore, a marked protection against oxidative stress was evident through reduction of lipid peroxidation and prevention of reduced glutathione content depletion and superoxide dismutase activity reduction in cardiac tissue of rats pretreated with sitagliptin in combination with doxorubicin. Moreover, sitagliptin ameliorated the activation of nuclear factor kappa-B and the release of inflammatory cytokines, tumour necrosis factoralpha and nitric oxide. Finally, sitagliptin attenuated doxorubicin-induced increase in the expression of pro-apoptotic protein Bax and in the apoptotic marker, caspase-3. Collectively, these data indicate that sitagliptin pretreatment could alleviate doxorubicininduced cardiotoxicity via reducing oxidative damage and its subsequent inflammation and apoptosis.

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“…12,14 Various mechanisms has been reported to be involved in doxorubicin induced cardiotoxicity. [15][16][17] However, its inhibitory effects on AMPK has been well documented. 4,11,16 Evidence has shown that AMPK is activated through adenine nucleotide dependent mechanism.…”

Section: Discussionmentioning

confidence: 99%

Effect of metformin on ECG, HR and BP of rats administered with cardiotoxic agent doxorubicin

Emeka

AlAhmed

2017

Int J Basic Clin Pharmacol

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Background: Cardiovascular complications during drug therapy is worrisome and has been known to increase morbidity and mortality. The aim of this study was to investigate the effect of metformin on BP, HR, and ECG, after subacute administration of doxorubicin in rats.Methods: Laboratory acclimatised animals were divided into 4 experimental groups consisting of group I as the control, given 0.5ml normal saline. Group II, received 3mg/kg doxorubicin on alternate days, while group III was given 300mg/kg metformin. The last group of animals were treated with 300mg/kg metformin, 30 min later, the animals were injected doxorubicin ip. The treatment lasted for 15 days thereafter, ECG, HR and BP were measured with anaesthesia.Results: Result showed that doxorubicin induced ECG changes in terms of increased PR and QT intervals significantly. Whereas, QRS and RR intervals were at same time significantly decreased. Metformin was observed to significantly attenuate these changes. In addition, metformin restored decreases in HR that was caused by doxorubicin in a significant fashion. However, metformin alone produced a decrease in HR compared with control. The observed reduced SBP and DBP produced by doxorubicin were also alleviated by the administration of metformin. There were increases in BP parameters measured in normotensive rats with metformin alone.Conclusions: In conclusion, metformin was found to attenuate doxorubicin-induced alteration in ECG pattern and restored the mechanical and physiological functions of the rat heart. Our data further suggests monitoring of CVS changes such as ECG particularly with drugs known to cause myocardial injury.

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Epigallocatechin-3-gallate pretreatment attenuates doxorubicin-induced cardiotoxicity in rats: A mechanistic study

Cited by 92 publications

References 87 publications

The Cardenolide Glycoside Acovenoside A Affords Protective Activity in Doxorubicin-Induced Cardiotoxicity in Mice

The Cardenolide Glycoside Acovenoside A Affords Protective Activity in Doxorubicin-Induced Cardiotoxicity in Mice

Cardioprotective effects of sitagliptin against doxorubicin-induced cardiotoxicity in rats

Effect of metformin on ECG, HR and BP of rats administered with cardiotoxic agent doxorubicin

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