Protective effect of Korean red ginseng extract on cisplatin ototoxicity in HEI‐OC1 auditory cells

Im, Gi Jung; Chang, Jiwon; Choi, June; Chae, Sung Won; Ko, Eun Ju; Jung, Hak Hyun

doi:10.1002/ptr.3082

Cited by 54 publications

(44 citation statements)

References 17 publications

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“…KRG extracts, or its specific saponins, were shown to have antiapoptotic and antioxidant properties in various tissues both in vitro and in vivo [8] . Recently, it was shown that KRG has otoprotective properties against gentamicin [9,10] , 3-nitropropionic acid [12] , and CDDP-induced ototoxicity [8,13] .…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it was shown that KRG has otoprotective properties against gentamicin [9,10] , 3-nitropropionic acid [12] , and CDDP-induced ototoxicity [8,13] . These studies revealed that KRG mainly works by inhibition of some proapoptotic genes such as caspase-1, caspase-3, and the TNF family of genes and by enhancement of antiapoptotic gene expression such as bcl-2 [8][9][10][11][12][13] . On the other hand, KRG has antiapoptotic effects on neuronal tissues [18] .…”

Section: Discussionmentioning

confidence: 99%

“…It was shown that this effect mainly works by up regulation of the p13K/Akt signaling pathway, which is a cell survival pathway. Activation of this pathway inhibits apoptosis by decreasing p53 and caspase-3 expression while also increasing expression of genes in the bcl2 family [8,11,18] . KRG has also been shown to be an otoprotective agent following cochlear injury associated with noise-induced hearing loss [25] .…”

Section: Discussionmentioning

confidence: 99%

“…KRG has been found to be effective in various problems that cause hearing loss such as gentamycin ototoxicity, age-related hearing loss, or 3-nitropropionic acid-induced cochlear damage [8][9][10][11][12] . CDDP-induced hearing loss has been studied in one in vitro and in one in vivo study [8,13] . The aim of this study was to evaluate the effects of different doses of KRG on CDDP ototoxicity both in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Korean Red Ginseng on Cisplatin Ototoxicity: Is It Effective Enough?

Olgun¹,

Kırkım²,

Altun³

et al. 2016

Int Adv Otol

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1 (HEI-OC1) cell line. Cells were treated with CDDP, KRG, and their combination for 24 h. Cell viability, apoptosis, and the expression of 84 apoptosis-related genes were analyzed. In the second part of the study, 30 Wistar albino rats were divided into five groups. Baseline distortion product otoacoustic emissions (DPOAEs) and auditory brainstem response (ABR) measurements were obtained. In groups I, II, and III, only saline, KRG, and CDDP, respectively, were given. In group IV, 500 mg/kg KRG and in group V, 150 mg/kg of KRG were administered for 10 days. In groups III, IV, and V, 16 mg/kg CDDP injections were administered on day 11. On day 14, final DPOAEs and ABR measurements were completed. The rats were then sacrificed, and their inner ear structures were evaluated by transmission electron microscopy. RESULTS:In the first part of the study, pretreatment with 1 mg/mL KRG protected cells from CDDP ototoxicity. This protection was mainly due to a decline in apoptotic gene expression and an increase in antiapoptotic gene expression. In the in vivo part of the study, we found that both KRG doses had otoprotective effects. This protection was more prominent at the lower dose, especially on the spiral ganglion and the brainstem.CONCLUSION: KRG was shown to be an otoprotective agent against CDDP-induced ototoxicity both in vivo and in vitro.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Korean Red Ginseng on Cisplatin Ototoxicity: Is It Effective Enough?

Olgun¹,

Kırkım²,

Altun³

et al. 2016

Int Adv Otol

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“…Cisplatin ototoxicity emerges as symmetrical hearing loss in which particularly high frequencies are irreversibly affected. Many antioxidant agents such as sodium thiosulfate, N-acetylcysteine, acetyl-L-carnitine, Korean red ginseng, and resveratrol have been tested in vitro and in vivo in order to prevent this irreversible side effect (3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Untitled

2017

Turk Arch Otorhinolaryngol

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Objective: Cisplatin is a widely used agent for the treatment of adult and childhood malignancies. Side effects such as nephrotoxicity, neurotoxicity, and ototoxicity lead to dose limitations. Ecklonia cava polyphenol extract (ECP) is a molecule obtained from algae that live in seawater in the Far East. ECP has recently been shown to have protective effects against oxidative stress. The aim of this study was to evaluate the possible protective effects of ECP on cisplatin ototoxicity. Methods:In this study, we investigated the protective effects of ECP against cisplatin-induced cell death in mouse-derived House Ear Institute Organ of Corti (HEI-OC1) cochlear cells. Cisplatin (100 µM) and 1, 10, and 25 µM doses of ECP were administered to the cells, and the protective effects of ECP at 24 and 72 hours were investigated. Cell viability was evaluated by the WST-1 (water soluble tetrazolium salt).Results: Cisplatin (100 µM) reduced cell viability in both the 24 th and 72 nd hour evaluation. Although the 25 µM dose of ECP showed otoprotective effects in the 24 th hour, in the 72 nd hour this effect disappeared. Other doses of ECP showed no otoprotective effects in the 24 th and 72 nd hours. Conclusion:Although ECP showed some protective effects in the 24 th hour against cisplatin ototoxicity, these effects disappeared by the 72 nd hour. Further studies using recurrent and higher doses of ECP are required.

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Protective effects of apocynin on cisplatin‐induced ototoxicity in an auditory cell line and in zebrafish

Choi

Chang

et al. 2011

J of Applied Toxicology

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Cisplatin is a very effective anticancer drug and generates reactive oxygen species (ROS) such as superoxide anions that can deplete antioxidant protective molecules in the cochlea. These processes result in the death of cochlear hair cells by induction of apoptosis. Apocynin, which is used as a specific nicotinamide adenine dinucleotide phosphate oxidase inhibitor, has a preventive effect for intracellular ROS generation. In this study, the effect of apocynin was investigated in a cochlear organ of Corti-derived cell line, HEI-OC1 cells, and in transgenic zebrafish (Brn3C: EGFP). To investigate the protective effects of apocynin, HEI-OC1 cells were treated with various concentrations of apocynin and a 20 µm concentration of cisplatin, simultaneously. An in vivo study of transgenic zebrafish (Brn3C: EGFP) was used to investigate the protective effects of apocynin on cisplatin-induced hair cell death. In an in vitro study, apocynin appeared to protect against cisplatin-induced apoptotic features on Hoechst 33258 staining in the HEI-OC1 cells. Treatment of the HEI-OC1 cells with 100 µm of apocynin, significantly decreased caspase-3 activity. Treatment of the cells with a 100 µm concentration of apocynin and a 20 µm concentration of cisplatin significantly decreased the intracellular ROS production. In the in vivo study, apocynin significantly decreased the TUNEL reaction and prevented cisplatin-induced hair cell loss of the neuromasts in the transgenic zebrafish at low concentrations (125 and 250 µm). These findings suggest that apocynin has antioxidative effects and prevents cisplatin-induced apoptotic cell death in HEI-OC1 cells as well as in zebrafish.

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Protective effect of Korean red ginseng extract on cisplatin ototoxicity in HEI‐OC1 auditory cells

Cited by 54 publications

References 17 publications

Protective Effect of Korean Red Ginseng on Cisplatin Ototoxicity: Is It Effective Enough?

Protective Effect of Korean Red Ginseng on Cisplatin Ototoxicity: Is It Effective Enough?

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Protective effects of apocynin on cisplatin‐induced ototoxicity in an auditory cell line and in zebrafish

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