Immunohistochemical and histological evaluations of cyclophosphamide-induced acute cardiotoxicity in wistar rats: The role of turmeric extract (curcuma)

Komolafe, O.A.; Arayombo, Babatunde Elijah; Abiodun, Adeleke Adegboyega; Saka, O.S.; Zabdiel, Abijo Ayodeji; Ojo, S.K.; Fakunle, O.O.

doi:10.1016/j.morpho.2019.10.047

Cited by 12 publications

(6 citation statements)

References 27 publications

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“…4 Our findings revealed a significant increase in MDA, the most important parameter in detecting oxidative stress, and significant decreases in GSH, SOD, and TAC, which is consistent with other models. [29][30][31]12 Inflammasomes are a type of protein complex that is formed to enhance immune responses and cause cellular damage. Several inflammasomes were described, including NLRP3, NLRP1, AIM2, and NLRC4.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…This pathway is highly involved in CYC-induced cardiac injury. [12][13][14][15] Recently, 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have become the essential treatment for dyslipidemia. Statins are mainly effective in decreasing both lowdensity lipoprotein cholesterol and, to a lesser extent, triglyceride levels.…”

Section: Introductionmentioning

confidence: 99%

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Simvastatin cardioprotection in cyclophosphamide-induced toxicity via the modulation of inflammasome/caspase1/interleukin1β pathway

et al. 2022

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Drug-induced cardiotoxicity is a serious adverse effect that occurs during the administration of chemotherapeutic agents such as cyclophosphamide (CYC). Therefore, there is a critical need to find cardioprotective agents to keep the heart healthy. The current study aimed to investigate the protective effect of simvastatin (SIM) against CYC-induced heart damage and evaluate different mechanisms involved in mediating this effect, including the inflammasome/caspase1/interleukin1β (IL1β) pathway and endothelial nitric oxide synthase (eNOS). 36 rats were randomly assigned to one of four groups: a control group that received only vehicles, a CYC group that received CYC (150 mg/kg/day) i.p. on the fourth and fifth days, a CYC+SIM group that received SIM (10 mg/kg/day) orally for 5 days and CYC (150 mg/kg/day) i.p. on the fourth and fifth days, and a CYC+SIM+ Nitro- ω-L-arginine (L-NNA) group that received L-NNA (25 mg/kg/day, SIM (10 mg/kg/day) orally for 5 days and CYC (150 mg/kg/day) i.p. on the 4th and 5th days. The CYC group revealed an obvious elevation in cardiac enzymes and heart weights with toxic histopathological changes. Moreover, there was an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNFα) levels, and up-regulation of the NLRP3inflammasome/caspase1/IL1β pathway. In addition, total antioxidant capacity (TAC), eNOS, reduced glutathione (GSH), and superoxide dismutase (SOD) significantly decreased. CYC-induced cardiotoxicity was most properly reversed by SIM through its anti-oxidant, anti-inflammatory, and anti-apoptotic actions with the stimulation of eNOS. The co-administration of L-NNA diminished the protective effect of SIM, indicating the essential role of eNOS in mediating this effect. Therefore, SIM ameliorated CYC-induced cardiotoxicity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Simvastatin cardioprotection in cyclophosphamide-induced toxicity via the modulation of inflammasome/caspase1/interleukin1β pathway

et al. 2022

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“…It is believed that these metabolites could induce oxidative stress and free radicals generation which may cause damage to capillary endothelial lining with resultant extravasation and leakage of erythrocytes, proteins, and free radicals which may cause further damage to myocardium and blood vessels 16 . Furthermore, it was found that treatment with CPD may cause inhibition of carnitine palmitoyl transferase-I gene expression and heart-type fatty acid-binding proteins in the heart 17 , such inhibition may lead to decrease energy production and result in fatty acid oxidation and free radicals generation with subsequent cardiac damage 17 . Moreover, CPD promotes the expression of proinflammatory cytokine 18 , enhances the phosphorylation of nuclear factorkappa B, TNF-α, IL-1β, and increases serum level of cyclooxygenase-2 which may cause multi-organ toxicity including heart, kidney, lung, and bone marrow 18 .…”

Section: Discussionmentioning

confidence: 99%

Study the Prophylactic Effects of Melatonin and Cyanocobalamin Against Cyclophosphamide-Induced Cardiotoxicity

Ghanim

Al-Moziel²,

Al-Yousof³

2022

Bulletin of Pharmaceutical Sciences. Assiut

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English Cyclophosphamide chemotherapeutic agent, it's used associated with multiorgan toxicity including the heart. Melatonin and cyanocobalamin possess cardiac-protective properties. This study was designed to evaluate the prophylactic effects of melatonin and cyanocobalamin. Fifty adult male rats have used in the study, divided into five groups each containing ten rats, melatonin, and cyanocobalamin were given orally for seven consecutive days before injection of (150 mg/kg) of cyclophosphamide on day seven. Group I: Control group, in which rats were intraperitoneally injected with (1 ml/kg/day) of normal saline. Group II: Rats were intraperitoneally injected with a single dose of cyclophosphamide. Group III: Rats were given orally melatonin at a dose (1 mg/kg/day) and cyclophosphamide. Group IV: Rats were given orally cyanocobalamin at a dose (0.1 mg/kg/day) and cyclophosphamide. Group V: Rats were administered orally a mixture of melatonin at a dose (1 mg/kg/day) and cyanocobalamin at a dose (0.1 mg/kg/day) and cyclophosphamide. On day eight rats were sacrificed, serum and heart extracted for malondialdehyde, interleukin-1 beta, and troponin I measurement, furthermore cardiac immunohistochemical study was performed. It was found that both melatonin and cyanocobalamin significantly (P<0.05) decrease serum levels of malondialdehyde, interleukin-1 beta, and troponin I in comparison with group II and improve immunohistochemical changes in cardiac tissue when compared with the group treated by cyclophosphamide only (group II).

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“…CP-intoxicated cardiomyocytes are responsible for increased synthesis of NADPH oxidase, NADH dehydrogenase, and NADPH oxidase. The activation of these enzymatic systems is associated with the generation of free radical-mediated oxidative stress [ 24 , 25 ]. The myocardial cell when exposed to CP treatment increases NADPH oxidase and other mediators of ROS.…”

Section: Mode Of Cardiotoxicity Inductionmentioning

confidence: 99%

Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics

Adhikari

Asdaq²,

Hawaj

et al. 2021

Pharmaceuticals

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The advancement in therapy has provided a dramatic improvement in the rate of recovery among cancer patients. However, this improved survival is also associated with enhanced risks for cardiovascular manifestations, including hypertension, arrhythmias, and heart failure. The cardiotoxicity induced by chemotherapy is a life-threatening consequence that restricts the use of several chemotherapy drugs in clinical practice. This article addresses the prevalence of cardiotoxicity mediated by commonly used chemotherapeutic and immunotherapeutic agents. The role of susceptible genes and radiation therapy in the occurrence of cardiotoxicity is also reviewed. This review also emphasizes the protective role of antioxidants and future perspectives in anticancer drug-induced cardiotoxicities.

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Immunohistochemical and histological evaluations of cyclophosphamide-induced acute cardiotoxicity in wistar rats: The role of turmeric extract (curcuma)

Cited by 12 publications

References 27 publications

Simvastatin cardioprotection in cyclophosphamide-induced toxicity via the modulation of inflammasome/caspase1/interleukin1β pathway

Simvastatin cardioprotection in cyclophosphamide-induced toxicity via the modulation of inflammasome/caspase1/interleukin1β pathway

Study the Prophylactic Effects of Melatonin and Cyanocobalamin Against Cyclophosphamide-Induced Cardiotoxicity

Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics

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