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Trichostatin A reduces cisplatin-induced ototoxicity through the STAT6 signaling pathway 期刊论文

编号：

66b8f592-d4b3-4785-a765-ebd2a67a8a5c
作者：

Huang, Ji#^[1]Wang, Ping(王苹)#^[2]Li, Min^[1];Ge, Jingyan^[3];Chen, Jiaqi^[1];Chen, Xia*^[1]
语种：

英文
期刊：

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE ISSN：1107-3756 2015 年 36 卷 2 期 (493 - 500) ; AUG
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关键词：

trichostatin A ototoxicity signal transducer and activator of transcription 6 inflammation
摘要：

Cisplatin-induced ototoxicity limits its wide application in the treatment of cancer. A number of pro-inflammatory factors have been shown to be involved in cisplatin-induced ototoxicity. Trichostatin A (TSA) is an anti-inflammatory agent that has been shown to exert protective effects against cisplatin-induced ototoxicity. In the present study, we hypothesized that TSA may protect cochlear hair cells from cisplatin-induced damage by regulating the interleukin (IL)-4/signal transducer and activator of transcription (STAT) 6 signaling pathway. Wistar rat cochlear explants were cultured in DMEM. The differentially expressed genes of the basilar membrane were identified by microarray analysis of global expression profiles. Hair cells were stained with rhodamine phalloidin and observed under a scanning electron microscope to evaluate the protective effects of TSA against cisplatin-induced cochlear hair cell damage. The levels of cytokines in the supernatant of the cultured basilar membranes was measured using ELISA. STAT6 and phosphorylated (p-) STAT6 expression was measured by western blot analysis. Morphological observation revealed that cisplatin induced the disarrangement of the cochlear hair cells, as well as the fusion and detachment of the cilia, while these aberrant alterations were inhibited by TSA, suggesting that TSA exerts a protective effect against cisplatin-induced damage to hair cells. Furthermore, the increase in the expression of STAT6 and p-STAT6 induced by cisplatin was reversed by treatment with TSA, accompanied by the decreased expression of IL-1 beta, IL-4 and IL-6. Therefore, our data demonstrate that TSA reduces cisplatin-induced ototoxicity by inhibiting pro-inflammatory factor-mediated STAT6 signaling. Thus, TSA may be used to prevent the side-effects associated with the use of cisplatin in cancer treatment.
推荐引用方式
GB/T 7714：

Huang Ji,Wang Ping,Li Min, et al. Trichostatin A reduces cisplatin-induced ototoxicity through the STAT6 signaling pathway [J].INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,2015,36(2):493-500.
APA：

Huang Ji,Wang Ping,Li Min,Ge Jingyan,&Chen Xia.(2015).Trichostatin A reduces cisplatin-induced ototoxicity through the STAT6 signaling pathway .INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,36(2):493-500.
MLA：

Huang Ji, et al. "Trichostatin A reduces cisplatin-induced ototoxicity through the STAT6 signaling pathway" .INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 36,2(2015):493-500.
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