Protective effects of caffeic acid phenethyl ester on doxorubicin‐induced cardiotoxicity in rats

Fadıllıoğlu, Ersin; Öztaş, Emin; Erdoğan, Hasan; Yagmurca, Murat; Söğüt, Sadık; Uçar, Muharrem; Irmak, M. Kemal

doi:10.1002/jat.945

Cited by 135 publications

(87 citation statements)

References 30 publications

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“…Parlakpınar et al (10) reported that CAPE acts in the heart as a potent scavenger of free radicals to prevent the apoptotic effect of myocardial ischemia/reperfusion injury. The authors showed that CAPE inhibits lipid peroxidation and suppresses oxidative stress (9,11). It was shown in the previous studies that CAPE preserved heart tissue from doxorubicin-induced cardiac damage (11).…”

Section: Introductionmentioning

confidence: 95%

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Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats

Oktar¹,

Aydın²,

Yönden³

et al. 2010

Anadolu Kardiyol Derg

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ÖZETAmaç: Kafeik asit fenetil ester (CAPE) güçlü antiinflamatuvar, anti-tümör ve antioksidan özelliklere sahip doğal bir üründür ve iskemireperfüzyonun indüklediği inflamasyonu ve lipid peroksidasyonu azaltır. Bu çalışmanın amacı isoproterenol (ISO) indüklü miyokardiyal infarktüs üzerine CAPE tedavisinin etkilerini incelemektir. Yöntemler: Bu çalışmada rasgele deneysel kontrollü araştırma dizaynı seçildi. Sıçanlar dört gruba ayrıldı: Kontrol, CAPE, ISO, ISO+CAPE. CAPE (10 μmol kg/gün i.p.) ve ISO (150 mg /kg s.c.) tek başlarına ratlara 7 gün süreyle verildi. ISO+CAPE grubunda ise ratlara ISO (150 mg /kg s.c.) uygulamasından 3 gün önce CAPE (10 μmol kg/gün i.p.) verilmeye başlandı. Yedi günlük deney periyodunun sonunda ratlar öldürüldü ve biyokimyasal analizler için kan ve doku örnekleri alındı. Verilerin istatistiksel analizi tek-yönlü ANOVA ve post-hoc LSD testi ile yapıldı. Bulgular: Tek başına ISO uygulanması sonucu myeloperoksidaz (MPO) aktivitesi, lipid peroksidasyonu, süperoksit dismutaz (SOD) ve katalaz (CAT) aktiviteleri arttı. Tek başına CAPE uygulaması ise enzim değerlerini kontrole göre değiştirmedi. CAPE tedavisi verilen grupta ise MPO aktivitesi ve malondialdehit seviyesi düşerken, CAT ve SOD aktivitesi değişmedi. Sonuç: Mevcut bulgular CAPE tedavisinin nötrofil MPO aktivitesini inhibe ederek MPO ve lipid peroksidasyon aracılı miyokardiyal hasarı önle-diğine işaret etmektedir. (Anadolu Kardiyol Derg 2010; 10: 298-302) Anahtar kelimeler: Kafeik asit fenetil ester, isoproterenol, lipid peroksidasyonu, miyokardiyal infarktüs, oksidatif stres, miyeloperoksidaz ABSTRACT Objective: Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor and antioxidant activities and attenuates inflammation and lipid peroxidation induced by ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on isoproterenol (ISO) -induced myocardial infarction. Methods: A randomized controlled experimental design was used in this study. Rats were divided into four groups and treated with saline, CAPE, ISO and ISO+CAPE. Rats were treated with CAPE (10 μmol kg/day i.p.) or saline starting 3 days before injecting ISO (150 mg /kg s.c., 24 hours). Seven days later, rats were sacrificed and the hearts were excised for biochemical analyses and microscopic examination. One-way ANOVA test with post hoc multiple comparisons using LSD method were used for statistical analysis of the data. Results: The administration of ISO alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities did not change in rat given CAPE alone. CAPE treatment prevented the increase in MPO activity and malondialdehyde, but did not affect the activities SOD and CAT enzymes. Conclusion: In light of these results, we conclude that CAPE prevents MPO-and lipid peroxidation-mediated myocardial injury via inhibition of neutrophil's MPO activity. (Anadolu Kardiyol Derg 2010; 10: 298-302)

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Section: Introductionmentioning

confidence: 95%

“…The authors showed that CAPE inhibits lipid peroxidation and suppresses oxidative stress (9,11). It was shown in the previous studies that CAPE preserved heart tissue from doxorubicin-induced cardiac damage (11).…”

Section: Introductionmentioning

confidence: 95%

Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats

Oktar¹,

Aydın²,

Yönden³

et al. 2010

Anadolu Kardiyol Derg

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“…A single dose administration of Dox (10 mg kg −1 ) caused a significant increase in MDA content (an index of lipid peroxidation) in cardiac tissues and decrease in myocardial GSH compared to control group indicating an increase in oxidative stress. (Fadillioglu et al, 2004;Patil and Balaraman, 2005). Administration of LSFJ improved the biochemical marker levels indicating decrease in oxidative stress as evident by increased level of GSH and SOD with decreased lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Lagenaria siceraria (Molina) Standley (Cucurbitaceae) Fruit Juice on Doxorubicin Induced Cardiotoxicity in Rats

Fard¹,

Naseh²,

Bodhankar³

et al. 2010

American J. of Pharmacology and Toxicology

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Problem statement:The cardio toxicity of Doxorubicin (Dox) has limited its use as an anticancer drug. The aim of present study was to investigate the cardio protective effect of Lagenaria Siceraria (Cucurbitaceous) Fruit Juice (LSFJ) against the cardio toxicity of Dox in rats. Approach: Male wistar rats (250-300 g) were randomly divided into four groups. Group I-was control, Group II-Dox (10 mg kg −1 ), groups III and IV-Dox + LSFJ (5 and 10 mL kg −1 for 18 days). Dox (10 mg kg −1 iv) was administered in group II, III and IV on day 16. After anesthetizing the animals on the 18th day, Electrocardiogram (ECG) was recorded and blood was investigated for Creatine Kinase-MB is enzyme (CK-MB), Lactate Dehydrogenase (LDH) and Aspartate Aminotransferase (AST) while determination of Superoxide Dismutase (SOD), Reduced Glutathione (GSH), Lipid Per Oxidation (LPO) and histopathology was carried out for heart. Results: Group 3 and 4 of animals showed decreased QT interval (p<0.05) and was non significant in ST interval and heart rate compared to Group 2. Significant decrease in serum CK-MB and AST of group 3 (p<0.05) and group 4(p<0.01) of animals was observed as compared to group II. In group 4 significant increase in the level of GSH (p<0.01) and decrease in MDA content (p<0.001) was observed as compared to group 2, whereas SOD was non-significant. Histopathological study of LSFJ10 mL kg −1 treated group showed protection against myocardial toxicity induced by doxorubicin. Conclusion: It is concluded that Lagenaria siceraria fruit juice possessed cardio protective effect at dose of 10 mL kg −1 against doxorubicin induced cardio toxicity in rats.

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“…Results of our study confirm the contribution of inflammation in DOX-induced cardiotoxicity, because anti-inflammatory agents can at least, in part, reduce DOX-induced cardiotoxicity. It has been suggested that DOX also induces endothelial dysfunctions (Kotamraju et al, 2002;Wolf and Baynes, 2006), because it has been demonstrated in vivo that treatment with DOX caused oxidative stress and myeloperoxidase (MPO) activity (Fadillioglu et al, 2004). N e -(carboxymethyl)lysine can be formed by oxidative stress (Baynes, 1991;Nerlich and Schleicher, 1999), and also by the enzyme MPO (Anderson et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory agents and monoHER protect against DOX-induced cardiotoxicity and accumulation of CML in mice

et al. 2007

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Cardiac damage is the major limiting factor for the clinical use of doxorubicin (DOX). Preclinical studies indicate that inflammatory effects may be involved in DOX-induced cardiotoxicity. N e -(carboxymethyl) lysine (CML) is suggested to be generated subsequent to oxidative stress, including inflammation. Therefore, the aim of this study was to investigate whether CML increased in the heart after DOX and whether anti-inflammatory agents reduced this effect in addition to their possible protection on DOX-induced cardiotoxicity. These effects were compared with those of the potential cardioprotector 7-monohydroxyethylrutoside (monoHER). BALB/c mice were treated with saline, DOX alone or DOX preceded by ketoprofen (KP), dexamethasone (DEX) or monoHER. Cardiac damage was evaluated according to Billingham. N e -(carboxymethyl) lysine was quantified immunohistochemically. Compared to saline, a 21.6-fold increase of damaged cardiomyocytes was observed in mice treated with DOX (Po0.001). Addition of KP, DEX or monoHER before DOX significantly reduced the mean ratio of abnormal cardiomyocytes in comparison to mice treated with DOX alone (Pp0.02). In addition, DOX induced a significant increase in the number of CML-stained intramyocardial vessels per mm 2 (P ¼ 0.001) and also in the intensity of CML staining (P ¼ 0.001) compared with the saline-treated group. N e -(carboxymethyl) lysine positivity was significantly reduced (Pp0.01) by DOX-DEX, DOX-KP and DOX-monoHER. These results confirm that inflammation plays a role in DOX-induced cardiotoxicity, which is strengthened by the observed DOX-induced accumulation of CML, which can be reduced by anti-inflammatory agents and monoHER.

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Protective effects of caffeic acid phenethyl ester on doxorubicin‐induced cardiotoxicity in rats

Cited by 135 publications

References 30 publications

Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats

Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats

Cardioprotective Effect of Lagenaria siceraria (Molina) Standley (Cucurbitaceae) Fruit Juice on Doxorubicin Induced Cardiotoxicity in Rats

Anti-inflammatory agents and monoHER protect against DOX-induced cardiotoxicity and accumulation of CML in mice

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