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通过声音预处理可抑制耳蜗中的细胞凋亡。

Suppression of apoptosis occurs in the cochlea by sound conditioning.

作者信息

Niu Xianzhi, Shao Ruijin, Canlon Barbara

机构信息

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Neuroreport. 2003 May 23;14(7):1025-9. doi: 10.1097/01.wnr.0000070830.57864.32.

Abstract

Apoptosis plays a critical role in the pathogenesis of noise-induced hearing loss. The goal of this study was to determine if apoptotic pathways are suppressed by sound conditioning. Sound conditioning is a pretreatment to low-level non-damaging sound that protects against a subsequent damaging acoustic trauma. Sound conditioning protects against hair cell death and thereby preserves hearing after a subsequent acoustic trauma. Using a combination of immunocytochemical and Western blotting techniques we show that acoustic trauma causes the release of cytochrome c from the mitochondria into the cytoplasm, and a decrease in bcl-2 immunoreactivity in the outer hair cells. Sound conditioning was found to trigger a protection against these detrimental changes. These data suggest that bcl-2 plays an important role in the regulation of hair cell death, and provides evidence that bcl-2 acts as an inducible neuroprotective gene that is upregulated by sound conditioning.

摘要

细胞凋亡在噪声性听力损失的发病机制中起关键作用。本研究的目的是确定细胞凋亡途径是否受到声音预处理的抑制。声音预处理是指对低强度无害声音进行预先处理,以保护免受随后的有害声损伤。声音预处理可防止毛细胞死亡,从而在随后的声损伤后保留听力。我们使用免疫细胞化学和蛋白质印迹技术相结合的方法表明,声损伤会导致细胞色素c从线粒体释放到细胞质中,并使外毛细胞中的bcl-2免疫反应性降低。发现声音预处理可触发对这些有害变化的保护作用。这些数据表明bcl-2在毛细胞死亡的调节中起重要作用,并提供证据表明bcl-2作为一种可诱导的神经保护基因,通过声音预处理上调。

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