Protective effect of tanshinone IIA against radiation-induced ototoxicity in HEI-OC1 cells
Author(s) -
Shasha Du,
Qiwei Yao,
Peixin Tan,
Guozhu Xie,
Chen Ren,
Quanquan Sun,
Xiao Zhang,
Rong Zheng,
Kaijun Yang,
Yawei Yuan,
Quan Yuan
Publication year - 2013
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2013.1486
Subject(s) - salvia miltiorrhiza , apoptosis , cell cycle , chemistry , ototoxicity , chromosomal translocation , pharmacology , mtt assay , cancer research , cell cycle checkpoint , nf κb , medicine , traditional chinese medicine , biochemistry , cisplatin , pathology , chemotherapy , alternative medicine , gene
Radiotherapy is a highly efficient treatment method for nasopharyngeal carcinoma that is often accompanied by significant ototoxic side-effects. The inner ear hair cells are particularly prone to serious injury following radiotherapy. Tanshinone IIA is a transcription factor inhibitor that is extracted from the traditional herbal medicine, Salvia miltiorrhiza Bunge. The present study investigated the effects of tanshinone IIA treatment on radiation-induced toxicity in the HEI-OC1 hair cell line. Using an MTT assay and flow cytometry, the radiation-induced weakening of the cells was observed to be alleviated when the cells were pre-treated with tanshinone IIA. Radiation exposure promoted p65/nuclear factor (NF)-κB nuclear translocation and activated the p53/p21 pathway, two processes which play a significant role in radiation-induced cell apoptosis. However, pre-treatment of the cells with tanshinone IIA inhibited p65/NF-κB nuclear translocation and p53/p21 pathway activation. These results demonstrate that tanshinone IIA is capable of protecting cochlear cells from radiation-induced injury through the suppression of p65/NF-κB nuclear translocation and the p53/p21 signaling pathway.
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