Cardioprotective Potential of Medicinal Plants in Attenuating Doxorubicin-Induced Cardiotoxicity
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Cardiotoxicity
Doxorubicin is a major culprit in chemotherapy-induced cardiotoxicity, which is the chief limiting factor in delivering optimal chemotherapy to cancer patients. Although extensive efforts have been devoted, no chemical synthesized drugs or natural compounds are available to prevent the harmful action of doxorubicin without reducing its anti-cancer efficacy. Accumulative experimental evidence has shown that polyphenols can prevent doxorubicin-induced cardiotoxicity largely due to their anti-cancer and cardio protective properties. We elaborated on the potential mechanisms associated with doxorubicin-induced cardiotoxicity and reviewed published literatures about the protective effects of polyphenols on doxorubicin-induced cardiotoxicity to provide novel strategies for the study of cardioprotective drugs.
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Doxorubicin/AE; Cardiomyopathies/CI; Phenols/PD; Review
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This study was aimed to investigate the protective effect of lignanoid against doxorubicin-induced cardiotoxicity in rats. Doxorubicin were administered at the dosage of 5 mg/kg once a week, ip for a period of 5 consecutive weeks. Lignanoid were administered at the dosages of 25, 50 and 100mg/kg, po by gavage for 7 consecutive days in a week for 5 weeks. Lignanoid at the doses of 50 and 100 mg/kg significantly reduced CK-MB, NO and LDH and increased GST levels in the doxorubicin-treated group. Thus, lignanoid ameliorated doxorubicin-induced cardiotoxicity by reducing oxidative stress, abnormal cellular morphology in rat. This study indicates the protective effect of lignanoid against doxorubicin-induced cardiotoxicity.
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This study investigated the cardioprotective effect of repeated remote ischemic preconditioning (rRIC) on doxorubicin-induced cardiotoxicity in mice.Doxorubicin is an effective chemotherapeutic agent for a wide range of tumor types but its use and dosing are limited by acute and chronic cardiotoxicity. Remote ischemic conditioning (RIC) is cardioprotective in multiple cardiovascular injury models, but the effectiveness of rRIC in doxorubicin-induced cardiotoxicity has not been fully elucidated.rRIC was performed on mice before and after doxorubicin administration. Cardiac function was assessed by echocardiography and myocardial biology was tested by molecular approaches.Doxorubicin administration induced acute cardiotoxicity, as indicated by reduced cardiac function, reduced myocyte cross-section area and increased extracellular collagen deposition, increased circulating cardiac muscle damage markers, and decreased heart weight. Doxorubicin also adversely affected other organs, including the kidney, liver, and spleen, as evaluated by circulating markers or organ weight loss. rRIC not only abrogated doxorubicin-induced cardiotoxicity (left ventricular ejection fraction, doxorubicin 47.5 ± 1.1%, doxorubicin + rRIC 51.6 ± 0.7%, p = 0.017), but also was associated with multiorgan protection. Within the myocardium, rRIC attenuated doxorubicin-induced cardiomyocyte apoptosis, reduced inflammation, and increased autophagy signaling.rRIC may be a promising approach to reduce doxorubicin-induced cardiotoxicity.
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Doxorubicin (Adriamycin) is an unquestionably effective anticancer agent for many types of tumors, including advanced breast cancer. However, cardiotoxic effects of the drug have limited its use. Methods of reducing or preventing doxorubicin-induced cardiotoxicity have been suggested, including an investigational doxorubicin analog, mitoxantrone ( Novantrone ). Mitoxantrone was developed to reduce the cardiotoxicity associated with doxorubicin while maintaining effective antitumoral effects. Initial reports suggested that mitoxantrone might lack cardiotoxic potential; however, recent studies indicate that the drug can produce adverse cardiac effects (congestive heart failure), perhaps with similar frequency to that observed with doxorubicin. It is doubtful that mitoxantrone will be a significant advance over doxorubicin if direct comparative studies reveal a similar incidence of cardiomyopathy.
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Abstract Background Doxorubicin (DOX) is widely used in lymphoma, myeloma, breast cancer, and other malignant tumors, and it significantly improves the prognosis of these patients. However, its side effects, especially cardiotoxicity, must be taken seriously. Studies have shown that liposome doxorubicin (L-DOX), compared with DOX, has increased anti-tumor activity and decreased cardiac toxicity. Our aim is to investigate the mechanism of myocardial injury in mice caused by these two drugs, to identify potential mitigation strategies. Methods In this study, mice or HL-1 cells were treated with DOX or L-DOX, and the cardiac morphology, hemodynamic effect, laboratory examination, and expression of ferritinophagy-related proteins were compared with the control group. Results DOX significantly induced myocardial cell death, while L-DOX had little effect on myocardial injury. Additionally, DOX significantly increased the level of autophagy and ferroptosis in cardiac myocytes. Further analysis revealed that NCOA4-mediated ferritinophagy played a key role in the mechanism of doxorubicin-induced cardiotoxicity (DIC). Importantly, the addition of ferrostatin-1 (a ferroptosis inhibitor) was able to rescue DIC. In contrast, L-DOX reduced the damage to cardiac myocytes by reducing ferritinophagy. Conclusion We have found that a significant relationship between the mechanism of DIC and NCOA4-mediated ferritinophagy. L-DOX has been shown to reduce the damage to myocardial cells by reducing NCOA4-mediated ferritinophagy. Thus, NCOA4 has the potential to be a drug target for the cardiac protection of DIC. However, further research is need to investigate the specific role of NCOA4 in the pathogenesis of DIC.
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Doxorubicin is a highly effective chemotherapeutic agent widely used to treat a variety of cancers. However, the clinical application of doxorubicin is limited due to its adverse effects on several tissues. One of the most serious side effects of doxorubicin is cardiotoxicity, which results in life-threatening heart damage, leading to reduced cancer treatment success and survival rate. Doxorubicin-induced cardiotoxicity results from cellular toxicity, including increased oxidative stress, apoptosis, and activated proteolytic systems. Exercise training has emerged as a non-pharmacological intervention to prevent cardiotoxicity during and after chemotherapy. Exercise training stimulates numerous physiological adaptations in the heart that promote cardioprotective effects against doxorubicin-induced cardiotoxicity. Understanding the mechanisms responsible for exercise-induced cardioprotection is important to develop therapeutic approaches for cancer patients and survivors. In this report, we review the cardiotoxic effects of doxorubicin and discuss the current understanding of exercise-induced cardioprotection in hearts from doxorubicin-treated animals.
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The study of mechanisms underlying cardiotoxicity of doxorubicin and the development of strategies to mitigate doxorubicin-induced cardiotoxicity are the most relevant issues of modern cardio-oncology. This is due to the high prevalence of cancer in the population and the need for frequent use of highly effective chemotherapeutic agents, in particular anthracyclines, for optimal management of cancer patients. However, while being a potent agent to counteract cancer, doxorubicin also affects the cardiovascular systems of patients undergoing chemotherapy in a significant and unfavorable fashion. Consecutively reviewed in this article are risk factors and mechanisms of doxorubicin cardiotoxicity, and the essential strategies to mitigate cardiotoxic effects of doxorubicin treatment in cancer patients are discussed.
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Doxorubicin is a potent anticancer agent effective in a wide range of malignancies, but its use is limited by dose-dependent late cardiotoxicity. Severe doxorubicin cardiotoxicity has been associated with a poor prognosis and a high mortality rate, and until recently has been thought to be irreversible. We describe the cases of three patients with well-documented severe left ventricular dysfunction due to doxorubicin who had complete clinical recovery with return of cardiac function to normal. Because severe doxorubicin cardiotoxicity is reversible in some patients, aggressive supportive therapy is warranted.
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Abstract: Background: Doxorubicin is an anthracycline anti-cancer drug and one of the most widely used chemotherapeutic medications to treat both solid and hematological tumors. However, due to the major adverse effect of cardiotoxicity, the clinical use of doxorubicin was highly restricted. Objectives: The current research was undertaken to explore the salutary properties of the triptonide on the doxorubicin-induced cardiotoxicity in rats. Materials and Methods: Rats were given 2.5 mg/kg of doxorubicin to produce cardiotoxicity, which was then treated with 25 mg/kg of triptonide. A set of rats was treated with 50 mg/kg of triptonide alone. Plethysmography on the tail-cuff was used to measure the blood pressure indicators. Using assay kits, the concentrations of oxidative and antioxidative biomarkers and cardiac function markers were measured. Using established techniques, the antioxidant enzyme activity was assessed. The histopathological study was performed on the heart tissues to analyze the doxorubicin-induced histological changes. Results: The heart weight was improved by triptonide treatment in the doxorubicin-induced rats. Triptonide effectively reduced the blood pressure indicators in the doxorubicin-induced rats. In the doxorubicin-induced rats, triptonide significantly decreased the LDH, CK, and AST activities and the status of myoglobin, H-FABP, GP-BB, and CK-MB. The triptonide therapy decreased the levels of INF-γ, MCP-1, and TGF-β in the serum of doxorubicin-induced rats. The findings of the histopathological examination showed that triptonide had therapeutic benefits. Conclusion: In summary, the results of this study supported the hypothesis that triptonide could ameliorate the biochemical and histological changes in the rats' hearts that were caused by doxorubicin. Keywords: Creatine kinase, Cardiac damage, Myoglobulin, Doxorubucin, Triptonide.
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