Niu Xianzhi, Shao Ruijin, Canlon Barbara
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Neuroreport. 2003 May 23;14(7):1025-9. doi: 10.1097/01.wnr.0000070830.57864.32.
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.
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。