Protective effect of resveratrol against cisplatin-induced ototoxicity in HEI-OC1 auditory cells

Lee, Se Hee; Kim, Hyung Sub; An, Yun Suk; Chang, Jiwon; Choi, June; Im, Gi Jung

doi:10.1016/j.ijporl.2014.11.008

Cited by 25 publications

(8 citation statements)

References 20 publications

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“…The efficacy of cisplatin in the clinic is limited by severe side effects in some cases but more prominently by tumor resistance [8]. The side effects of cisplatin include nephrotoxicity, ototoxicity, neurotoxicity and other side effects common to chemotherapy [9], [10], [11].…”

Section: Introductionmentioning

confidence: 99%

The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines

2017

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Cisplatin is a widely used chemotherapeutic drug showing high efficiency in the treatment of primary tumors such as ovarian, testicular and cervical cancers. The major drawback of cisplatin is tumor resistance either acquired or intrinsic. Many mechanisms are involved in the resistance, among them is the Nrf2 pathway which regulates glutathione related enzymes. Caffeic acid, a non-toxic polyphenol which is abundant in many foods modulates glutathione S-transferase (GST) and glutathione reductase (GSR) activity, these enzymes were shown to be involved in resistance of cells towards cisplatin. Caffeic acid induces the Nrf2 pathway and can also inhibit the activity of GST and GSR.Our findings demonstrate that the co-treatment of cancer cells with cisplatin and caffeic acid can enhance cisplatin cytotoxicity and increases the amount of platinum bound to nuclear DNA. However, 6 h of pre incubation with caffeic acid prior to cisplatin treatment led to acquired resistance to cisplatin and reduced DNA binding.In conclusion, the enzyme inhibitory action of caffeic acid is dominant when the two agents are co-administered leading to increased cytotoxicity, and the Nrf2 induction is dominant when the cells are treated with caffeic acid prior to cisplatin treatment leading to resistance.The use of caffeic acid as adjuvant for cisplatin should be carefully examined due to different pharmacokinetic profiles of caffeic acid and cisplatin. Thus, it is questionable if the two agents can reach the tumors at the right time frame in vivo.

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Section: Introductionmentioning

confidence: 99%

The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines

2017

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“…The cells were cultured in high-glucose Dulbecco’s Modified Eagle’s Medium (DMEM; Gibco BRL, Grand Island, NY, USA) containing 10% fetal bovine serum (FBS; JRH Bioscience, Lexena, KS, USA) and 50 U/mL interferon-γ without antibiotics at 33.8 °C and 10% CO 2 in air. The cell culture used the method of previously reported study [12].…”

Section: Methodsmentioning

confidence: 99%

Protective effect of agmatine against cisplatin-induced apoptosis in an auditory cell line

Park

Lee

et al. 2020

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23Objectives: Agmatine, an endogenous metabolite of arginine, is known to have 24 antioxidant activity, protect mitochondrial function, and confer resistance to cellular 25 apoptosis. The aim of this study was to evaluate the protective effects of agmatine 26 against cisplatin-induced cellular apoptosis in an auditory cell line. 27 Methods: HEI-OC1 cells were co-treated with agmatine at different concentrations and 28 15 µM cisplatin for 48 h. Cell viability was measured and annexin V-FITC/propidium 29 iodide (PI) staining was performed to analyze apoptosis. The levels of intracellular 30 reactive oxygen species (ROS) were measured using flow cytometry. The expression 31 of BAX (Bcl2-associated X protein) and the enzymatic activity of caspase-3 were 32 measured to examine the pathway of apoptosis induction. 33 Results: Co-treatment with 8 mM agmatine protected HEI-OC1 cells against cisplatin-34 induced cell apoptosis. Agmatine exerted a significant protective effect against 15 µM 35 cisplatin when applied for 48 h and reduced the proportion of necrotic and late 36 apoptotic cells. Agmatine did not reduce the cisplatin-induced increase in ROS but 37 decreased the expression of BAX and the activity of caspase-3. 38 Conclusions: Agmatine protected against cisplatin-induced cellular apoptosis in an 39 auditory cell line. These effects were mediated by the protection of mitochondrial 40 function and inhibition of apoptosis. 128 ChemiDOC touch imaging system (Bio-Rad, Hercules, CA). The relative band 129 densities were computed using ImageJ software (Imagej.nih.gov/ij/index.html).

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“…In this study, oral administration of resveratrol (5, 15, or 45 mg/kg/day for 10 days) protected against cisplatin-induced cardiotoxicity in adult male Wistar rats by alleviating cisplatin-induced oxidative stress [136]. However, resveratrol has been shown to protect against cisplatin-induced nephrotoxicity [137,138,139], gonadotoxicity [140,141,142], and ototoxicity [143,144,145]. Pretreatment with resveratrol did not significantly alter the plasma level of cisplatin; however, it lowered its urinary concentration and its accumulation in the kidneys, which may explain its protective effects [146].…”

Section: Other Cardiotoxic Cancer Treatmentsmentioning

confidence: 99%

Leveraging the Cardio-Protective and Anticancer Properties of Resveratrol in Cardio-Oncology

2019

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Cardio-oncology is a clinical/scientific discipline which aims to prevent and/or treat cardiovascular diseases in cancer patients. Although a large number of cancer treatments are known to cause cardiovascular toxicity, they are still widely used because they are highly effective. Unfortunately, therapeutic interventions to prevent and/or treat cancer treatment-induced cardiovascular toxicity have not been established yet. A major challenge for such interventions is to protect the cardiovascular system without compromising the therapeutic benefit of anticancer medications. Intriguingly, the polyphenolic natural compound resveratrol and its analogs have been shown in preclinical studies to protect against cancer treatment-induced cardiovascular toxicity. They have also been shown to possess significant anticancer properties on their own, and to enhance the anticancer effect of other cancer treatments. Thus, they hold significant promise to protect the cardiovascular system and fight the cancer at the same time. In this review, we will discuss the current knowledge regarding the cardio-protective and the anticancer properties of resveratrol and its analogs. Thereafter, we will discuss the challenges that face the clinical application of these agents. To conclude, we will highlight important gaps of knowledge and future research directions to accelerate the translation of these exciting preclinical findings to cancer patient care.

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Protective effect of resveratrol against cisplatin-induced ototoxicity in HEI-OC1 auditory cells

Cited by 25 publications

References 20 publications

The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines

The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines

Protective effect of agmatine against cisplatin-induced apoptosis in an auditory cell line

Leveraging the Cardio-Protective and Anticancer Properties of Resveratrol in Cardio-Oncology

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