Folic acid ameliorates celecoxib cardiotoxicity in a doxorubicin heart failure rat model

Ahmad, Shafique; Panda, Bibhu Prasad; Kohli, Kanchan; Fahim, Mohammad; Dubey, Kiran

doi:10.1080/13880209.2017.1299768

Cited by 34 publications

(20 citation statements)

References 50 publications

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“…Recent studies often research models that use DOX 6 times every other day at 2.5 mg/kg ( Merlet et al, 2013 ; Lončar-Turukalo et al, 2015 ; Cappetta et al, 2017a ; Ahmad et al, 2017 ; Cappetta et al, 2017b ; Elhadidy et al, 2020 ). Histological examination showed that this injection protocol results in irregularly spaced myocardial fibers with inflammation, edema, and leukocyte cell infiltration.…”

Section: Anthracycline Cardiomyopathy Modelsmentioning

confidence: 99%

Analysis of Models of Doxorubicin-Induced Cardiomyopathy in Rats and Mice. A Modern View From the Perspective of the Pathophysiologist and the Clinician

et al. 2021

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Today the pharmacological possibilities of treating cancer are expanding and as a result, life expectancy is increasing against the background of chemotherapy and supportive treatment. In the conditions of successful antitumor treatment, complications associated with its toxic effect on healthy tissues and organs began to come to the fore. Anthracycline cardiomyopathy was the first serious cardiovascular complication to draw the attention of oncologists and cardiologists around the world. Anthracycline drugs such as doxorubicin, epirubicin, idarubicin are still widely used in oncological practice to treat a wide range of solid and hematological malignancies. Doxorubicin-induced cardiomyopathy is closely associated with an increase in oxidative stress, as evidenced by reactive oxygen species (ROS) nduced damage such as lipid peroxidation, and decreased levels of antioxidants. Myofibrillar destruction and dysregulation of intracellular calcium are also important mechanisms, usually associated with doxorubicin-induced cardiotoxicity. Despite the abundance of data on various mechanisms involved in the implementation of doxorubicin-induced cardiotoxicity, a final understanding of the mechanism of the development of doxorubicin cardiomyopathy has not yet been formed. It poses the most significant challenges to the development of new methods of prevention and treatment, as well as to the unambiguous choice of a specific treatment regimen using the existing pharmacological tools. In order to resolve these issues new models that could reflect the development of the chemotherapy drugs effects are needed. In this review we have summarized and analyzed information on the main existing models of doxorubicin cardiomyopathy using small laboratory animals. In addition, this paper discusses further areas of research devoted to the development and validation of new improved models of doxorubicin cardiomyopathy suitable both for studying the mechanisms of its implementation and for the preclinical drugs effectiveness assessment.

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Section: Anthracycline Cardiomyopathy Modelsmentioning

confidence: 99%

Analysis of Models of Doxorubicin-Induced Cardiomyopathy in Rats and Mice. A Modern View From the Perspective of the Pathophysiologist and the Clinician

et al. 2021

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“…CVb3 infection of mouse hearts is routinely detected by the activities of biochemical markers, virus expression levels and histological changes on the heart on day 8 pi. Ck and Ldh are the most commonly used biochemical markers (ghormade et al, 2014;Ahmad et al, 2017). in this study, mice were inoculated with CVb3 to induce myocarditis, and then received nCC by oral gavage daily.…”

Section: Discussionmentioning

confidence: 99%

In vitro and in vivo antiviral activity of a fluoronucleoside analog, NCC, against Coxsackie virus B3

Wang¹,

Zhuan²,

Peng³

et al. 2021

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Coxsackie virus b3 (CVb3) is believed to be a major cause of viral myocarditis, with virusinduced apoptosis playing an important role in pathogenesis. The purpose of this study was to characterize the antiviral activity of a novel fluoronucleoside analogue, n-cyclopropyl-4'-azido-2'-deoxy-2'-fluoroβ-d-cytidine (nCC), against CVb3 in vitro and in vivo, and to establish whether nCC inhibits apoptosis in infected cells. in this study, heLa cells infected with CVb3 were treated with nCC. Cell viability and apoptosis were examined. Caspase-3 and bcl-2 levels were monitored by real-time RT PCR and Western blot analysis. for in vivo studies, bALb/c mice infected with CVb3 were treated with nCC daily. Serum markers of myocardial injury and histological studies were measured to examine myocardial injury on day 8 post infection. To measure apoptosis, levels of bcl-2 and caspase-3 were examined by immunohistochemistry and real-time RT-PCR. We found that nCC inhibited virus-mediated cytopathic effects in heLa cells with an eC 50 of 116.60 ± 0.32 μm. in infected mice, administration of nCC (2 mg/kg) decreased the activities of serum creatine kinase and lactic dehydrogenase, inhibited the replication of CVb3 and alleviated damage to the heart. importantly, nCC suppressed CVb3-induced apoptosis in heLa cells and affected the expression of apoptosis-related factors in infected mice. Together, our results demonstrate that nCC exerts significant antiviral activities against CVb3. We conclude that nCC is a potential therapeutic agent for the treatment of viral myocarditis.

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“…The HF injury model in vivo was generated as previously reported (21). After 12 weeks, rats were administered with 6 equal intraperitoneal injections of 2.5 mg/kg doxorubicin (DOX; Fresenius Kabi Oncology Ltd.) over a period of 2 weeks.…”

Section: Reverse Transcription-quantitative Polymerase Chain Reaction (Rt-qpcr)mentioning

confidence: 99%

BMP‑2 alleviates heart failure with type 2 diabetes mellitus and doxorubicin‑induced AC16 cell injury by inhibiting NLRP3 inflammasome‑mediated pyroptosis

Zhang

et al. 2021

Exp Ther Med

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Chronic heart failure (CHF) and diabetes mellitus are associated with morbidity and mortality. CHF and diabetes generally simultaneously occur, resulting in adverse outcomes. Diabetes complicates cardiomyopathy and exacerbates heart failure conditions. An increase in natriuretic peptides, including atrial natriuretic peptide (ANP), and another endsogenously generated peptide, brain natriuretic peptide (BNP), serves an essential role in CHF. The aim of this study was to explore the molecular regulation between bone morphogenetic protein-2 (BMP-2) and ANP or BNP in diabetes-associated cardiomyopathy. In total, 25 serum samples were collected from patients with CHF with or without type 2 diabetes mellitus to compare with 25 controls. Cardiomyopathy and hyperglycemia were induced in rats by doxorubicin and streptozotocin, respectively. AC16 cells were used to study molecular mechanisms. BMP, ANP and BNP concentration in patients and rats were measured by ELISA. Flow cytometry was performed to analyze cell pyroptosis and ROS production. Reverse transcription-quantitative PCR and western blotting were used to examine mRNA and protein expression of NOD-, LRR-and pyrin domain-containing protein 3 (NLRP3), pro-caspase-1, caspase-1 (p20) and gasdermin D. BMP-2 was negatively correlated with ANP and BNP in CHF patients with type 2 diabetes mellitus. Similar results were obtained in rats and AC16 cells. BMP-2 decreased the NLRP3 inflammasome activation and cell pyroptosis. The present study found evidence that the cardioprotective effects of BMP-2 act through ANP and BNP both in vivo and in vitro. BMP-2 inhibits inflammasome formation. The results suggested that BMP-2 may serve as a novel therapeutic target for the treatment of diabetic heart conditions.

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Folic acid ameliorates celecoxib cardiotoxicity in a doxorubicin heart failure rat model

Cited by 34 publications

References 50 publications

Analysis of Models of Doxorubicin-Induced Cardiomyopathy in Rats and Mice. A Modern View From the Perspective of the Pathophysiologist and the Clinician

Analysis of Models of Doxorubicin-Induced Cardiomyopathy in Rats and Mice. A Modern View From the Perspective of the Pathophysiologist and the Clinician

In vitro and in vivo antiviral activity of a fluoronucleoside analog, NCC, against Coxsackie virus B3

BMP‑2 alleviates heart failure with type 2 diabetes mellitus and doxorubicin‑induced AC16 cell injury by inhibiting NLRP3 inflammasome‑mediated pyroptosis

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