The influence of ginger administration on cisplatin-induced cardiotoxicity in rat: Light and electron microscopic study

El-Hawwary, Amany A.; Omar, Nesreen Moustafa

doi:10.1016/j.acthis.2019.04.013

Cited by 33 publications

(32 citation statements)

References 54 publications

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“…However, involvement of various signaling pathways including ER stress as well as non-nucleus-dependent apoptotic signal stimulation have been recently demonstrated [ 13 ]. Besides, some experimental studies suggested a direct damaging effect of CP on the cardiomyocyte [ [22] , [23] , [24] ]. Therefore, the current study aims on clarifying the underlying mechanism of CP-induced cardiotoxicity through ER-stress mediated apoptotic death in rats and the role of statins namely; RSV and SMV, in counteracting the CP detrimental effects on the cardiac tissue.…”

Section: Discussionmentioning

confidence: 99%

“…This leads to massive reactive oxygen species formation (ROS); eventually causing redox stress [ 7 , 8 ]. Oxidative stress initiates myocardial cell damage via endoplasmic reticulum (ER) stress activation resulting in severe cardiotoxicity [ 9 ]. The well-organized functioning of the ER is vital for different cellular activities; ER is an intracellular Ca 2+ storage organelle and among the most notable protein-folding compartments.…”

Section: Introductionmentioning

confidence: 99%

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Rosuvastatin and simvastatin attenuate cisplatin-induced cardiotoxicity via disruption of endoplasmic reticulum stress-mediated apoptotic death in rats: targeting ER-Chaperone GRP78 and Calpain-1 pathways

2020

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Cisplatin (CP) is a powerful antineoplastic chemotherapeutic agent with broad-spectrum properties. Acute and cumulative cardiotoxicity are major limiting factors for CP therapy. Various pathogenic pathways have been suggested to CP-induced cardiotoxicity; oxidative damage, ER stress, and programmed cell death/apoptosis. The present study aimed to assess the signaling mechanisms related to the advantageous effects of rosuvastatin (RSV) and simvastatin (SMV) against CP-related cardiac ER stress dependent apoptotic death in rats. Acute cardiotoxicity was induced by a single dose of CP (10 mg/kg, i.p.) on the 10th day of the experiment. RSV (10 mg/ kg/day) and SMV (10 mg/kg/day) were orally administered for 15 days. CP-treated rats showed significant alterations in electrocardiographic recordings and elevation in serum cardiac function biomarkers; troponin T content, lactate dehydrogenase and creatine kinase-MB levels as well as boost in the cardiac oxidative stress biomarkers. In addition, CP exposure resulted in GRP78 induction; an ER stress and elevation marker at calpain-1 content as well as activation of activated caspase-3 (ACASP3) and caspase-12 were reflected on CP-triggered apoptosis evidenced by elevation in the Bax/Bcl-2 ratio. However, RSV and SMV administration mitigate those adverse CP effects. Statins administration prominently alleviated CP-induced cardiac abnormalities exerting improvement in the ECG pattern and cardiac enzyme biomarkers. Interestingly, statins; RSV and SMV, disrupted CP-induced ER stress and the consequent apoptotic cell death evidenced by downregulation of ER-chaperone GRP78, calpain-1, ACASP3 and caspase-12 as well as decline in the Bax/Bcl-2 ratio. From all the previous findings, it can be suggested that statins namely; RSV and SMV, play protective role against CP-induced cardiac injury by regulating ER stress-mediated apoptotic pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rosuvastatin and simvastatin attenuate cisplatin-induced cardiotoxicity via disruption of endoplasmic reticulum stress-mediated apoptotic death in rats: targeting ER-Chaperone GRP78 and Calpain-1 pathways

2020

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“…It unleashes its anticancer action through formation of cisplatin‐DNA adduct by intrastrand cross‐links due to interaction with cancer cell DNA purine bases eventually leading to p53 activation, cell cycle arrest and induction of apoptosis (Calcabrini, Maffei, Turrini, & Fimognari, 2020; Dasari & Bernard Tchounwou, 2014). Despite its potent antineoplastic efficacy, the constraint to its clinical utility is the development of organ toxicity, including nephrotoxicity, neurotoxicity, hepatotoxicity, myelosuppression, cardiotoxicity, pancreatic and testicular damage (Bami et al., 2017; Bilgic et al., 2018; El‐Hawwary & Omar, 2019; Stošić et al., 2020). In the emerging papers, CIS‐induced damage to testes and hormonal imbalance has been suggested a chief side effect because it has been clinically associated with infertility (Altuner, Gulaboglu, Yapca, & Cetin, 2013; Mercantepe, Unal, Tümkaya, & Yazici, 2018; Sabanegh & Ragheb, 2009).…”

Section: Introductionmentioning

confidence: 99%

Ginger juice prevents cisplatin‐induced oxidative stress, endocrine imbalance and NO/iNOS/NF‐κB signalling via modulating testicular redox‐inflammatory mechanism in rats

Famurewa¹,

Ekeleme‐Egedigwe²,

Onwe

et al. 2020

Andrologia

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Chemotherapy is a cornerstone option in cancer treatment owing to its efficacy and effect on quality of life of cancer patients. The action mechanism of anticancer agents is targeted at deregulating cell cycle machinery and inhibiting unscheduled proliferation of cancer cells (Lin et al., 2020). Unfortunately, chemotherapeutic anticancer drugs often exert deleterious effect on healthy cells and tissues leading to systemic toxicity (Negrette-Guzmán, 2019). The toxicity may become unbearable that the treatment regimen has to be disrupted, even when achieving tumoricidal efficacy (Lin et al., 2020). Cisplatin (CIS) is an efficacious anticancer agent; it is the first choice for the treatment of advanced nonsmall-cell lung cancer cells, breast cancer and ovarian cancer (Browning et al., 2017; Lin et al., 2020; Manohar & Leung, 2018). It is of significant value also in the treatment of germ cell and testicular cancers (Thurston, 2007). It unleashes its anticancer action through formation of cisplatin-DNA adduct by intrastrand cross-links due to interaction with cancer cell DNA purine bases eventually leading to p53 activation, cell cycle arrest and induction

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“…The cisplatin alone-treated group showed disorganized cardiac muscle fibers appear, interrupted myofibrils, inflamed mitochondria, widen intercalated discs and elevated serum CK and LDH levels shown. 48 Additionally, cyclophosphamide treatment caused increased troponin I levels and increased levels of oxidative markers. However, no abnormality in troponin I and oxidative markers levels were seen in adult male albino rats that were treated with ginger and cyclophosphamide combination.…”

Section: -Gingerolmentioning

confidence: 99%

Protective Effect of Natural Products against Chemotherapy-Induced Cardiotoxicity: A Review

Othman¹,

Lum²,

Gan³

et al. 2020

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To complete this review, relevant literatures were searched from several scientific databases including Google, Google Scholar, Scopus, Web of Science and Pubmed. The categories of keywords used for searching are "Natural Products" or "Phytoconstituents" or "Isolated Compounds" or "Natural Compounds" or "Curcumin" or "Mangiferin" or "Naringenin" or "Quercetin" or "6-Gingerol" or "Lycopene" or "Resveratrol" or "Apigenin" or "Proanthocyanidins" or "Indole-3carbinol" and "Cardioprotection" or "Anticancer" or "Chemotherapy" or "Cardiotoxicity" or "Cardiotonic". After screening of literatures from 2005 to 2019, a total of ten natural products investigated the protective effect against chemotherapy-induced cardiotoxicity and that were included in the present review.

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The influence of ginger administration on cisplatin-induced cardiotoxicity in rat: Light and electron microscopic study

Cited by 33 publications

References 54 publications

Rosuvastatin and simvastatin attenuate cisplatin-induced cardiotoxicity via disruption of endoplasmic reticulum stress-mediated apoptotic death in rats: targeting ER-Chaperone GRP78 and Calpain-1 pathways

Rosuvastatin and simvastatin attenuate cisplatin-induced cardiotoxicity via disruption of endoplasmic reticulum stress-mediated apoptotic death in rats: targeting ER-Chaperone GRP78 and Calpain-1 pathways

Ginger juice prevents cisplatin‐induced oxidative stress, endocrine imbalance and NO/iNOS/NF‐κB signalling via modulating testicular redox‐inflammatory mechanism in rats

Protective Effect of Natural Products against Chemotherapy-Induced Cardiotoxicity: A Review

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