Cardioprotective effect of cannabidiol in rats exposed to doxorubicin toxicity

Fouad, Amr A.; Albuali, Waleed H.; Al-Mulhim, Abdulruhman S.; Jresat, Iyad

doi:10.1016/j.etap.2013.04.018

Cited by 93 publications

(68 citation statements)

References 38 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: 70%

“…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: Introductionsupporting

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: 70%

Section: Introductionsupporting

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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“…Mantawy et al found that ADR caused glutathione depletion, lipid peroxidation, and a reduction in activities of anti-oxidant enzymes that are indicators of oxidative stress; it also increased the expression of NF-κB and TNF-α levels which is an indicator of inflammation and induced apoptotic tissue damage by increasing Bax and cytochrome C and caspase-3 activity in heart tissue and resulted in cardiotoxicity [11]. Besides, Fouad et al studied cardiotoxic effects of ADR, and they revealed that NF-κB and caspase-3 levels were significantly increased in ADR-administrated rats [26].…”

Section: Discussionmentioning

confidence: 96%

Counteraction of Apoptotic and Inflammatory Effects of Adriamycin in the Liver Cell Culture by Clinopitolite

Yapışlar

Taşkın

Ozdas

et al. 2015

Biol Trace Elem Res

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Growing evidence has been reported on adriamycin (ADR) hepatotoxicity in literature. Hepatotoxicity caused by the use of drugs has a serious undesirable effect in the cure of cancer patients that needs to be eliminated. The exact mechanism of ADR on non-cancerous tissue still remains to be a mystery. The zeolite (clinoptilolite) minerals form a complex group of aluminosilicates that often occur as accessory minerals in intermediate and basic rocks. In light of this information, we investigated the possible anti-inflammatory and anti-apoptotic effects of clinoptilolite in ADR that is inducing the toxicity in primary liver cell culture. Primary liver cell culture from rat was used in the study. We had three experiment groups including the following: (1) cells treated only with 50 μM ADR for 24 h, (2) cells treated with the 50 μM ADR for 24 h and then treated with 10(-4) M zeolite for 1 h, and (3) cells were incubated with 50 μM ADR for 24 h and then incubated with 10(-4) M zeolite for 24 h to test its long-term effects. After that, western blotting was performed in order to evaluate protein expression levels of several inflammation markers including IL-1β, tumor necrosis factor (TNF)-α, and nuclear factor kappa B (NF-κB), and immunohistochemistry was carried out to detect apoptosis in liver cell culture. Also, TdT-dUTP Terminal Nick-End Labeling (TUNEL) method was used for detecting apoptosis. We found elevated levels of inflammatory protein and apoptotic markers in ADR-administered cells (p < 0.05). Inflammatory and apoptotic markers decreased significantly after treated with zeolite (p < 0.05). The present study was pointed out that ADR causes hepatotoxicity via apoptosis and/or inflammation processes resulting from initiator NF-κB and TNF which causes proinflammatory mediators such as IL-1β. Elevation of inflammation might give rise to trigger apoptosis. Clinoptilolite counteracted the apoptosis and inflammation induced by ADR arising from the decrease in NF-κB, TNF-α, and IL-1β protein levels.

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“…The doses of doxorubicin used in this study were based previous reports [19]. Rats in the treadmill training group underwent treadmill training, which began at 2 weeks after first intraperitoneal injection.…”

Section: Aerobic Exercise and Biochemical Analysismentioning

confidence: 99%

Effects of aerobic exercise on antioxidants in rat models with cardiomyopathy

Kim

2015

PTRS

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Objective: In this study, we aimed to test the hypothesis that aerobic exercise might exert its cardio-protective effect by preventing oxidative stress and improving cardiac function in rat models with doxorubicin-induced cardiomyopathy. Design: Randomized controlled trial. Methods: We randomly divided experimental rats into four groups: the normal group was used as a non-cardiomyopathy normal control (n=10); the control group included non-aerobic exercise after doxorubicin-induced cardiomyopathy (n=10); the experimental group I included aerobic exercise (3 m/min) after doxorubicin-induced cardiomyopathy (n=10); and experimental group II included aerobic exercise (8 m/min) after doxorubicin-induced cardiomyopathy. Rats in the treadmill training groups underwent treadmill training, which began at 2 weeks after the first intraperitoneal injection. At the end of the exercise period, we determined the heart weight change for each rat. Changes in the levels of oxidative stress enzymes (superoxide dismutase [SOD], thiobarbituric acid-reactive substances [TBARS], and catalase) in the cardiac tissue of rats from all four groups were examined at the end of the experiment. Results: Significant cardiac myocyte injury and increase in myocardial TBARS concomitant with a reduction in myocardial SOD and catalase were observed following cardiomyopathy (p<0.05). Significant cardiac tissue and increase in myocardial TBARS along with reduction in myocardial SOD and catalase were observed following cardiomyopathy (p<0.05). Oxidative parameters were significantly improved in the aerobic exercise groups compared with the control group. Conclusions: These findings indicate that aerobic exercise effectively prevents oxidative stress in rat models with cardiomyopathy.

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Cardioprotective effect of cannabidiol in rats exposed to doxorubicin toxicity

Cited by 93 publications

References 38 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

Counteraction of Apoptotic and Inflammatory Effects of Adriamycin in the Liver Cell Culture by Clinopitolite

Effects of aerobic exercise on antioxidants in rat models with cardiomyopathy

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