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氯化钴通过上调低氧诱导因子-1α预防噪声暴露小鼠的听力损失。

Up-regulation of hypoxia-inducible factor-1 alpha by cobalt chloride prevents hearing loss in noise-exposed mice.

机构信息

Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.

出版信息

Environ Toxicol Pharmacol. 2011 Jan;31(1):153-9. doi: 10.1016/j.etap.2010.10.002. Epub 2010 Oct 16.

DOI:10.1016/j.etap.2010.10.002
PMID:21787680
Abstract

Since hypoxia-inducible factor-1α (HIF-1α) is the key transcription factor that enables cells to survive in hypoxia, we have investigated whether an upregulation of HIF-1α prevents the noise-induced hearing loss in BALB/c hybrid mice, which were intraperitoneally injected with CoCl(2) (a HIF-1α inducer) and exposed to white band noise with 120 dB peak equivalent sound pressure level for 3h once daily for 3 days. In the CoCl(2) treatment group, HIF-1α was found to be up-regulated in the cochlear tissues and the hearing loss was largely prevented. Histologically, the loss of sensory hair cells was also significantly lower in the CoCl(2) treatment group than the Control group. However, YC-1 (a HIF-1α inhibitor) attenuated the preventive effect of CoCl(2) on the noise-induced hearing loss. These results suggest that HIF-1α plays a crucial role in the prevention against noise trauma in the inner ear.

摘要

由于缺氧诱导因子-1α(HIF-1α)是使细胞在缺氧环境中存活的关键转录因子,我们研究了上调 HIF-1α 是否可以预防 BALB/c 杂交小鼠的噪声性听力损失,这些小鼠通过腹腔注射 CoCl₂(HIF-1α 诱导剂),并在每天接受 3 小时、峰值等效声压级为 120dB 的白噪声暴露。在 CoCl₂处理组中,发现 HIF-1α 在耳蜗组织中上调,听力损失得到了很大程度的预防。组织学上,CoCl₂处理组的感觉毛细胞丢失也明显低于对照组。然而,YC-1(HIF-1α 抑制剂)减弱了 CoCl₂对噪声性听力损失的预防作用。这些结果表明,HIF-1α 在预防内耳噪声损伤中起着至关重要的作用。

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