Protective effects of deep sea water against doxorubicin-induced cardiotoxicity in H9c2 cardiac muscle cells

Lee, Do‐Hyung; Kim, Soyoung; Nam, Kyung‐Soo

doi:10.3892/ijo.2014.2666

Cited by 7 publications

(5 citation statements)

References 37 publications

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“…DOX is an anthracycline antibiotic and broad spectrum anti-cancer agent [6,7]. Although DOX is useful for the treatment of triple-negative breast cancer (TNBC), in practice its use is limited because of its serious side effects, which include cardiotoxicity, diarrhea, vomiting, hair loss, and nausea.…”

Section: Introductionmentioning

confidence: 99%

“…Although DOX is useful for the treatment of triple-negative breast cancer (TNBC), in practice its use is limited because of its serious side effects, which include cardiotoxicity, diarrhea, vomiting, hair loss, and nausea. Actually, the total dose of DOX administered must not exceed 450-500 mg/m 2 because of its cardiotoxicity [6]. Furthermore, reductions in DOX dosage made to address its side effects reduce its therapeutic efficacy [8].…”

Section: Introductionmentioning

confidence: 99%

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Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells

Lee

Kwon

et al. 2020

IJMS

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Several reports have described the anti-cancer activity of arctigenin, a lignan extracted from Arctium lappa L. Here, we investigated the effect of arctigenin (ATG) on doxorubicin (DOX)-induced cell death using MDA-MB-231 human breast cancer cells. The results showed that DOX-induced cell death was enhanced by ATG/DOX co-treatment in a concentration-dependent manner and that this was associated with increased DOX uptake and the suppression of multidrug resistance-associated protein 1 (MRP1) gene expression in MDA-MB-231 cells. ATG enhanced DOX-induced DNA damage and decreased the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and the expressions of RAD51 and survivin. Cell death caused by ATG/DOX co-treatment was mediated by the nuclear translocation of apoptosis inducing factor (AIF), reductions in cellular and mitochondrial Bcl-2 and Bcl-xL, and increases in mitochondrial BAX levels. However, caspase-3 and -7 did not participate in DOX/ATG-induced cell death. We also found that DOX/ATG-induced cell death was linked with activation of the p38 signaling pathway and suppressions of the phosphorylations and expressions of Akt and c-Jun N-terminal kinase. Taken together, these results show that ATG enhances the cytotoxic activity of DOX in MDA-MB-231 human breast cancer cells by inducing prolonged p21 expression and p38-mediated AIF-dependent cell death. In conclusion, our findings suggest that ATG might alleviate the side effects and improve the therapeutic efficacy of DOX.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells

Lee

Kwon

et al. 2020

IJMS

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“…However, the clinical use of this valuable anticancer drug is limited by severe toxic side effects on the heart, which may result in heart failure (2). Numerous studies have implicated reactive oxygen species generation in the cardiotoxicity of DOX, which ultimately results in cardiomyocyte apoptosis (3,4). A number of pharmacological interventions have been proposed as therapies to oppose DOX-induced cardiotoxicity, including resveratrol (RES) and oleanolic acid (5,6).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol inhibits doxorubicin-induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes

Liu

Shan

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it can induce severe cytotoxicity, which limits its clinical application. In the present study, the effects of resveratrol (RES) on sirtuin 1 (SIRT1) activation in mediating DOX-induced cytotoxicity in H9c2 cardiac cells was investigated. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX cardiotoxicity. Apoptosis of H9c2 cardiomyocytes was assessed using the MTT assay and Hoechst nuclear staining. The results demonstrated that pretreating H9c2 cells with RES prior to the exposure of DOX resulted in increased cell viability and a decreased quantity of apoptotic cells. Western blot analysis demonstrated that DOX decreased the expression level of SIRT1. These effects were significantly alleviated by co-treatment with RES. In addition, the results demonstrated that DOX administration amplified forkhead box O1 (FoxO1) and P53 expression levels in H9c2 cells. RES was also found to protect against DOX-induced increases of FoxO1 and P53 expression levels in H9c2 cells. Furthermore, the protective effects of RES were arrested by the SIRT1 inhibitor nicotinamide. In conclusion, the results demonstrated that RES protected H9c2 cells against DOX-induced injuries via SIRT1 activation.

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“…In previous reports, DSW has been shown to prevent atherosclerosis [ 20 ], attenuate the level of plasma lipid and adipogenic protein expression [ 21 ], and inhibit visceral fat accumulation and liver steatosis [ 22 ]. Furthermore, we previously demonstrated that DSW has anti-cancer metastatic [ 23 ], cardioprotective [ 24 ], and hypocholesterolemic effects [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Refined Deep-Sea Water Suppresses Inflammatory Responses via the MAPK/AP-1 and NF-κB Signaling Pathway in LPS-Treated RAW 264.7 Macrophage Cells

Chun

Lee

Nam

2017

IJMS

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Atopic dermatitis (AD) is a type of inflammatory skin disease caused by genetics, immune system dysfunction, and environmental stresses. It is, however, still considered to be a refractory disease. Macrophages are inflammatory immune cells that infiltrate the skin and induce inflammation. We investigated the effect of refined deep-sea water (RDSW) on lipopolysaccharide (LPS)-induced inflammatory response in RAW 264.7 macrophage cells. The results showed that RDSW suppressed the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2. Furthermore, nitric oxide, a product of iNOS, and prostaglandin (PG) D2 and PGE2, products of COX-2, were significantly inhibited by RDSW in a hardness-dependent manner. Moreover, we found that RDSW reversed the release of histamines and regressed the mRNA expressions and production of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-10, and vascular endothelial growth factor, in a hardness-dependent manner. We also found that the suppressive effect of RDSW on LPS-induced inflammatory responses was regulated by the inhibition of NF-κB nuclear translocation, and ERK 1/2 and JNK 1/2 mediated the suppression of c-Jun and c-Fos expressions. In conclusion, the present investigation suggests the possibility that RDSW may be used to treat and/or prevent inflammatory diseases, including AD.

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Protective effects of deep sea water against doxorubicin-induced cardiotoxicity in H9c2 cardiac muscle cells

Cited by 7 publications

References 37 publications

Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells

Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells

Resveratrol inhibits doxorubicin-induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes

Refined Deep-Sea Water Suppresses Inflammatory Responses via the MAPK/AP-1 and NF-κB Signaling Pathway in LPS-Treated RAW 264.7 Macrophage Cells

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