Cranberry (Vaccinium macrocarpon) protects against doxorubicin-induced cardiotoxicity in rats

Elberry, Ahmed A.; Abdel-Naim, Ashraf B.; Abdel‐Sattar, Essam; Nagy, Ayman A.; Mosli, Hisham A.; Mohamadin, Ahmed M.; Ashour, Osama M.

doi:10.1016/j.fct.2010.02.008

Cited by 100 publications

(59 citation statements)

References 58 publications

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“…31 These results are in accordance with the previous investigations. [32][33][34] Sitagliptin pretreatment counteracted these ECG abnormalities in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 96%

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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“…31 These results are in accordance with the previous investigations. [32][33][34] Sitagliptin pretreatment counteracted these ECG abnormalities in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 96%

Cardioprotective effects of sitagliptin against doxorubicin-induced cardiotoxicity in rats

El‐Agamy

Abo‐Haded

Elkablawy

2016

Exp Biol Med (Maywood)

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“…[2][3][4][5][6][7][8][9][10][11][12]34 In our study, serum markers that indicate cardiac, hepatic, and renal damage increased significantly 4 days after 30 mg kg À1 DOX was administered, compared with the controls. In the light microscopic examination, histopathologic changes were seen in tissues of the DOX-treated rats.…”

Section: Discussionmentioning

confidence: 80%

Beneficial effects of carnosine and carnosine plus vitamin E treatments on doxorubicin-induced oxidative stress and cardiac, hepatic, and renal toxicity in rats

et al. 2015

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Objective: Oxidative stress plays an important role in doxorubicin (DOX)-induced toxicity. Carnosine (CAR) is a dipeptide with antioxidant properties. The aim of this study was to evaluate the decreasing or preventive effect of CAR alone or combination with vitamin E (CAR + Vit E) on DOX-induced toxicity in heart, liver, and brain of rats. Methods: Rats were treated with CAR (250 mg kg−1 day−1; intraperitoneally (i.p.)) or CAR + Vit E (equals 200 mg kg−1 α-tocopherol; once every 3 days; intramuscularly) for 12 consecutive days. On the 8th day of treatment, rats were injected with a single dose of DOX (30 mg kg−1, i.p.). Serum cardiac troponin I (cTnI), urea, and creatinine levels; alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; and oxidative stress parameters in tissues were measured. We also determined thiobarbituric acid reactive substances, diene conjugate, protein carbonyl (PC), and glutathione levels and antioxidant enzyme activities. Results: DOX resulted in increased serum cTnI, ALT, AST, urea, and creatinine levels and increased lipid peroxide and PC levels in tissues. CAR or CAR + Vit E treatments led to decreases in serum cTnI levels and ALT and AST activities. These treatments reduced prooxidant status and ameloriated histopathologic findings in the examined tissues. Conclusion: Our results may indicate that CAR alone, especially in combination with Vit E, protect against DOX-induced toxicity in heart, liver, and kidney tissues of rats. This was evidenced by improved cardiac, hepatic, and renal markers and restoration of the prooxidant state and amelioration of histopathologic changes.

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“…Therefore, SOD and CAT play an important role in the elimination of ROS [43]. The reduction in the activities of antioxidant enzymes can be elucidated on the basis of their exhaustion against oxidative damages [44]. …”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice

Taghiabadi

Imenshahidi

Abnous

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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Reactive α,β-unsaturated aldehydes such as acrolein (ACR) are major components of environmental pollutants and have been implicated in the neurodegenerative and cardiac diseases. In this study, the protective effect of silymarin (SN) against cardiotoxicity induced by ACR in mice was evaluated. Studies were performed on seven groups of six animals each, including vehicle-control (normal saline + 0.5% w/v methylcellulose), ACR (7.5 mg/kg/day, gavage) for 3 weeks, SN (25, 50 and 100 mg/kg/day, i.p.) plus ACR, vitamin E (Vit E, 100 IU/kg, i.p.) plus ACR, and SN (100 mg/kg, i.p.) groups. Mice received SN 7 days before ACR and daily thereafter throughout the study. Pretreatment with SN attenuated ACR-induced increased levels of malondialdehyde (MDA), serum cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB), as well as histopathological changes in cardiac tissues. Moreover, SN improved glutathione (GSH) content, superoxide dismutase (SOD), and catalase (CAT) activities in heart of ACR-treated mice. Western blot analysis showed that SN pretreatment inhibited apoptosis provoked by ACR through decreasing Bax/Bcl-2 ratio, cytosolic cytochrome c content, and cleaved caspase-3 level in heart. In conclusion, SN may have protective effects against cardiotoxicity of ACR by reducing lipid peroxidation, renewing the activities of antioxidant enzymes, and preventing apoptosis.

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Cranberry (Vaccinium macrocarpon) protects against doxorubicin-induced cardiotoxicity in rats

Cited by 100 publications

References 58 publications

Cardioprotective effects of sitagliptin against doxorubicin-induced cardiotoxicity in rats

Cardioprotective effects of sitagliptin against doxorubicin-induced cardiotoxicity in rats

Beneficial effects of carnosine and carnosine plus vitamin E treatments on doxorubicin-induced oxidative stress and cardiac, hepatic, and renal toxicity in rats

Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice

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