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首页> 外文期刊>Oncology letters >Protective effect of tanshinone IIA against radiation-induced ototoxicity in HEI-OC1 cells
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Protective effect of tanshinone IIA against radiation-induced ototoxicity in HEI-OC1 cells

机译:丹参酮IIA对HEI-OC1细胞辐射诱导的耳毒性的保护作用

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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 p65uclear 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.
机译:放射疗法是鼻咽癌的一种高效治疗方法,通常伴有明显的耳毒性副作用。放射疗法后,内耳毛细胞特别容易受到严重伤害。丹参酮IIA是一种转录因子抑制剂,是从传统草药丹参中提取的。本研究调查了丹参酮IIA处理对HEI-OC1毛细胞系辐射诱导的毒性的影响。使用MTT测定法和流式细胞仪,当用丹参酮IIA预处理细胞时,观察到减轻了辐射诱导的细胞减弱。辐射暴露促进p65 /核因子(NF)-κB核易位并激活p53 / p21途径,这两个过程在辐射诱导的细胞凋亡中起着重要作用。但是,用丹参酮IIA预处理细胞会抑制p65 /NF-κB核移位和p53 / p21途径活化。这些结果表明,丹参酮IIA能够通过抑制p65 /NF-κB核易位和p53 / p21信号通路来保护耳蜗细胞免受辐射诱导的伤害。

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