Doxorubicin mediated cardiotoxicity in rats: Protective role of felodipine on cardiac indices

Gandhi, Hardik; Patel, Vaibhav B.; Mistry, Nirav; Patni, N. J.; Nandania, Jatin; Balaraman, R

doi:10.1016/j.etap.2013.07.007

Cited by 21 publications

(13 citation statements)

References 45 publications

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“…Pretreatment with SA and CAP significantly ameliorated the loss in these parameters, reflecting the cardioprotection that they can elicit and align with the results of previous studies [32][33][34]. CAP is used as a standard cardioprotective agent against DOX-induced cardiotoxicity [15].…”

Section: Discussionsupporting

confidence: 87%

Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

Jardan

Ansari

Raish

et al. 2020

BioMed Research International

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In the present study, we explored SA’s activity against DOX-induced cardiotoxicity and revealed its underlying mechanisms. Male Wistar rats (weight, 190-210g; n=6) were randomly divided into four groups: group I, normal control; group II, DOX 15 mg/kg via intraperitoneal (ip) route; group III, administered DOX+SA 20 mg/kg; and group IV, administered DOX+captopril (CAP 30 mg/kg). SA and CAP were administered orally for seven days, and DOX (15 mg/kg) was injected intraperitoneally an hour before SA treatment on the fifth day. Forty-eight hours after DOX administration, animals were anesthetized and sacrificed for molecular and histology experiments. SA significantly mitigated the myocardial effects of DOX, and following daily administration, it reduced serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB to near normal values. Levels of oxidative stress markers, glutathione-peroxidase, superoxide dismutase, and catalase, in the cardiac tissue were significantly increased, whereas malondialdehyde levels decreased after SA treatment in DOX-administered rats. Furthermore, DOX caused an inflammatory reaction by elevating the levels of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and endothelin- (ET-) 1, as well as nuclear factor kappa-B (NF-κB) expression. Daily administration of SA significantly repressed TNF-α, IL-1β, ET-1, and NF-κB levels. caspase-3 and Bax expression, bcl-2-like protein and caspase-3 activities and levels. Overall, we found that SA could inhibit DOX-induced cardiotoxicity by inhibiting oxidative stress, inflammation, and apoptotic damage.

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Section: Discussionsupporting

confidence: 87%

Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

Jardan

Ansari

Raish

et al. 2020

BioMed Research International

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“…In the present study, DOX administration to hypertensive rats showed a decrease in SBP, increase in LVEDP and decrease in LV dP/dtmax, denoting a reduction in cardiac functions especially myocardial contractility. These findings are in accordance with previous studies (Warpe et al, 2015;Gandhi et al, 2013). These changes were associated with development of oxidative stress as evidenced by a decrease in SOD levels, increase in MDA and myocardial damage which was evidenced by a significant increase in serum CK-MB.…”

Section: Discussionsupporting

confidence: 93%

Melatonin combination with perindopril alleviated doxorubicin cardiac toxicity in L-NAME hypertensive rats: comparative study with perindopril

Salam

El-Bakly

Badawy

et al. 2020

Ain Shams Journal of Forensic Medicine and Clinical Toxicology

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Introduction: Doxorubicin is a highly effective anticancer agent with serious cardiotoxic effects. Hypertension is considered as a major risk factor for doxorubicin cardiotoxicity. It should be noted that about one-third of cancer patients have hypertension, and melatonin can have cardio-protective effects. The present study aimed to further investigate the possible beneficial effects of melatonin co-administration to perindopril against doxorubicin cardiotoxicity in hypertensive rats. Method: Rats were randomly assigned to naïve group and N-Omega-Nitro-L-Arginine Methyl Ester Hydrochloride (L-NAME) hypertensive group. L-NAME group was further subdivided into untreated, doxorubicin, doxorubicin / perindopril, doxorubicin/melatonin and doxorubicin/ perindopril / melatonin subgroups. Cardiac functions, CK-MB, malondialdehyde, superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), and cardiac percentage area of collagen fibers were evaluated. Results: Combining melatonin with perindopril to doxorubicin produced significant decreases in left ventricular end diastolic pressure, malondialdehyde, TNF-α, and TGF-β. It resulted in significant increases in left ventricular dP/dtmax and SOD, in addition to apparent improvement in cardiac histopathology with a significant decrease in percentage area of collagen deposition compared to perindopril alone. Conclusion: Co-administration of melatonin to perindopril in hypertensive rats who received doxorubicin alleviated doxorubicin cardiac toxicity more than using perindopril alone. These effects could be explained by the reported antihypertensive, anti-inflammatory, anti-oxidant, and antifibrotic effects of melatonin.

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“…Similar results were obtained by previous studies [Richard et al, 2011;Colak et al, 2012;Warpe et al, 2015]. ECG revealed significant prolongation of QT interval in DOX-administered groups (II, III) as reported by Rahimi_Balaei et al [2010]; Ashour et al [2011] and Warpe et al [2015]; denoting delayed repolarization and a negative chronotropic effect [Gandhi et al, 2013] or metabolic and electrolyte abnormalities associated with developed heart failure [Hunter et al, 2008].…”

Section: Discussionsupporting

confidence: 88%

Functional and Structural Assessment of the Effect of Human Umbilical Cord Blood Mesenchymal Stem Cells in Doxorubicin‐Induced Cardiotoxicity

Allah

Hussein

Hasan

et al. 2017

J of Cellular Biochemistry

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Cardiomyopathy induced by doxorubicin (DOX) was recognized at an early stage and also several years after drug administration. Mesenchymal stem cells (MSCs) have many properties that make them suitable for preventive and/or regenerative therapies. In this study, we evaluated the effect of MSCs in the functional and the structural improvement of DOX-induced cardiomyopathy in rats. Ninety adult male albino rats were randomly divided into three equal groups of thirty rats each: Group I (control): rats received normal saline. Group II (DOX- group): rats received DOX. Group III (DOX-MSCs group): rats received DOX for 2 weeks then human umbilical cord blood mesenchymal stem cells (hUCB-MSCs). Rats in all groups were evaluated for: physical condition, electrocardiography (ECG), and hemodynamic parameters. Serum cardiac troponin I (cTnI), malondialdehyde (MDA), total antioxidant capacity (TAC), and DNA fragmentation on heart tissue isolated DNA were estimated for evaluation of the mechanism and the extent of the damage. Hearts were examined histopathologically for detection of MSCs homing, structural evaluation, with counting of the collagen fibers for evaluation of fibrosis. DOX-administered rats showed significant functional and structural deterioration. DOX-MSCs treated rats (group III) showed improved functional and structural criteria with restoration of all biochemical indicators of cardiac damage and reactive oxygen species (ROS) to normal, as well. In Conclusion, hUCB-MSCs significantly ameliorated the cardiotoxic manifestations as shown by biochemical, functional, and structural cardiac improvement. J. Cell. Biochem. 118: 3119-3129, 2017. © 2017 Wiley Periodicals, Inc.

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Doxorubicin mediated cardiotoxicity in rats: Protective role of felodipine on cardiac indices

Cited by 21 publications

References 45 publications

Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

Melatonin combination with perindopril alleviated doxorubicin cardiac toxicity in L-NAME hypertensive rats: comparative study with perindopril

Functional and Structural Assessment of the Effect of Human Umbilical Cord Blood Mesenchymal Stem Cells in Doxorubicin‐Induced Cardiotoxicity

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