Sung Il Cho1, Ji-Eun Lee2, Nam Yong Do2. 1. Department of Otolayngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea. Electronic address: chosi@chosun.ac.kr. 2. Department of Otolayngology-Head and Neck Surgery, Chosun University School of Medicine, Gwangju, South Korea.
Abstract
OBJECTIVES: Silymarin is a plant extract with strong antioxidant properties in addition to anti-inflammatory and anticarcinogenic actions. The aim of this study was to investigate the potential preventive effect of silymarin on cisplatin ototoxicity in an auditory cell line, HEI-OC1 cells. METHODS: Cultured HEI-OC1 cells were exposed to cisplatin (30 μM) with or without pre-treatment with silymarin (50 μM). Cell viability was evaluated using MTT assay. Hoechst 33258 staining was used to identify cells undergoing apoptosis. Western blot analysis was done to evaluate whether silymarin inhibits cisplatin-induced caspase and PARP activation. Cell-cycle analysis was done by flow cytometry to investigate whether silymarin is capable of protecting cisplatin-induced cell cycle arrest. RESULTS: Cell viability significantly increased in cells pretreated with silymarin compared with cells exposed to cisplatin alone. Pre-treatment of silymarin appeared to protect against cisplatin-induced apoptotic features on Hoechst 33258 staining. Cisplatin increased cleaved caspase-3 and PARP on Western blot analysis. However, pre-treatment with silymarin inhibited the expression of cleaved caspase-3 and PARP. Silymarin did attenuate cell cycle arrest and apoptosis in HEI-OC1 cells. CONCLUSIONS: Our results demonstrate that silymarin treatment inhibited cisplatin-induced cytotoxicity in the auditory cell line, HEI-OC1. Silymarin may be a potential candidate drug to eliminate cisplatin induced ototoxicity.
OBJECTIVES:Silymarin is a plant extract with strong antioxidant properties in addition to anti-inflammatory and anticarcinogenic actions. The aim of this study was to investigate the potential preventive effect of silymarin on cisplatinototoxicity in an auditory cell line, HEI-OC1 cells. METHODS: Cultured HEI-OC1 cells were exposed to cisplatin (30 μM) with or without pre-treatment with silymarin (50 μM). Cell viability was evaluated using MTT assay. Hoechst 33258 staining was used to identify cells undergoing apoptosis. Western blot analysis was done to evaluate whether silymarin inhibits cisplatin-induced caspase and PARP activation. Cell-cycle analysis was done by flow cytometry to investigate whether silymarin is capable of protecting cisplatin-induced cell cycle arrest. RESULTS: Cell viability significantly increased in cells pretreated with silymarin compared with cells exposed to cisplatin alone. Pre-treatment of silymarin appeared to protect against cisplatin-induced apoptotic features on Hoechst 33258 staining. Cisplatin increased cleaved caspase-3 and PARP on Western blot analysis. However, pre-treatment with silymarin inhibited the expression of cleaved caspase-3 and PARP. Silymarin did attenuate cell cycle arrest and apoptosis in HEI-OC1 cells. CONCLUSIONS: Our results demonstrate that silymarin treatment inhibited cisplatin-induced cytotoxicity in the auditory cell line, HEI-OC1. Silymarin may be a potential candidate drug to eliminate cisplatin induced ototoxicity.
Authors: Ovidiu Horea Bedreag; Alexandru Florin Rogobete; Mirela Sărăndan; Alina Cradigati; Marius Păpurică; Oana Maria Roşu; Corina Maria Dumbuleu; Dorel Săndesc Journal: Rom J Anaesth Intensive Care Date: 2014-10