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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Molecular mechanisms underlying cochlear degeneration in the tubby mouse and the therapeutic effect of sulforaphane.
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Molecular mechanisms underlying cochlear degeneration in the tubby mouse and the therapeutic effect of sulforaphane.

机译：海豚鼠耳蜗变性的分子机制和萝卜硫烷的治疗作用。

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As with Usher syndrome observed in humans, the two main phenotypes of the tubby mouse are progressive hearing loss and retinal degeneration. Yet, the mechanism underlying the tub-related cochlear degeneration is still unclear. The reduction/oxidation (redox) imbalance in the cell is related to many kinds of diseases. This study examined expressions of thioredoxin (Trx) and Trx reductase (TrxR), an important redox system in the cell, and the related upstream and downstream proteins of the Trx/TrxR in the tubby mouse cochlea. This report also examined the therapeutic effect of sulforaphane (SF) on the cochlear degeneration, which showed a protective effect on the tub-related retinal degeneration in our previous report. The results showed that the tub-mutation resulted in a significant suppression of Trx and TrxR expressions. Expression level of Nrf2 (NFE2 related factor 2), a transcription factor that regulates expression of Trx and TrxR and others, was also suppressed in the tubby mouse cochlea. Furthermore, a lowered level of activated extracellular signal-regulated kinase (p-ERK) was observed in the tubby mouse cochlea. In contrast, caspase-3 expression and activity were enhanced in the tubby mouse, suggesting apoptotic cell death. The tub-related molecular alterations in the cochlea were prevented by chronic treatment with SF. As a result, the SF-treatment significantly delayed the tub-related cochlear degeneration. Other unknown proteins may contribute to tubby-related degeneration because Nrf2 regulates many other antioxidants besides Trx/TrxR and sulforaphane did not prevent cochlear degeneration completely although it completely prevented alterations of Nrf2 and Trx/TrxR.
机译：与在人类中观察到的Usher综合征一样，大白鼠的两个主要表型是进行性听力丧失和视网膜变性。然而，与桶相关的耳蜗变性的潜在机制仍不清楚。细胞中的还原/氧化（氧化还原）失衡与多种疾病有关。这项研究检查了硫氧还蛋白（Trx）和Trx还原酶（TrxR）（一种重要的细胞氧化还原系统）的表达以及Trx / TrxR的相关上下游蛋白在海豚小鼠耳蜗中的表达。该报告还研究了萝卜硫素（SF）对耳蜗变性的治疗作用，在我们以前的报告中显示对肾小管相关的视网膜变性具有保护作用。结果表明，tub突变导致Trx和TrxR表达的显着抑制。 Nrf2（NFE2相关因子2）的表达水平，一种调节Trx和TrxR及其它表达的转录因子，在海豚鼠耳蜗中也受到抑制。此外，在矮胖的小鼠耳蜗中观察到了较低水平的活化的细胞外信号调节激酶（p-ERK）。相比之下，caspase-3的表达和活性在大白鼠中得到增强，提示凋亡细胞死亡。 SF的慢性治疗可防止耳蜗中与盆相关的分子改变。结果，SF治疗显着延迟了与桶相关的耳蜗变性。其他未知蛋白可能会导致与海豚相关的变性，因为Nrf2调节除Trx / TrxR之外的许多其他抗氧化剂，而萝卜硫烷虽然可以完全阻止Nrf2和Trx / TrxR的改变，但不能完全阻止耳蜗变性。

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