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首页> 外文期刊>Journal of International Medical Research >Effects of D-methionine in mice with noise-induced hearing loss mice
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Effects of D-methionine in mice with noise-induced hearing loss mice

机译:D-蛋氨酸对噪声性听力损失小鼠的影响

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Objective To study the effects of D-methionine in a mouse model of noise-induced hearing loss (NIHL). Methods We investigated changes in auditory function and microscopic cochlear structure in a mouse model of NIHL, and carried out 4-hydroxynonenal (4-HNE) immunostaining and terminal deoxynucleotidyl transferase dUTP nick-end labeling, and examined expression levels of connexins 26 and 30 by western blot. Results The auditory brainstem response threshold was significantly increased by noise exposure. Noise exposure also damaged the inner and particularly the outer hair cells in the cochlear basement membrane, while histochemistry demonstrated only scattered loss of hair cells in the basement membrane in mice treated with D-methionine before or after noise exposure. D-methionine inhibited apoptosis in the cochlear basement membrane, stria vascularis, and spiral ligament. 4-HNE expression in the basement membrane, stria vascularis, and spiral collateral ligament was increased by noise exposure, but this increase was attenuated by D-methionine. Connexin 26 and connexin 30 expression levels were reduced by noise exposure, and this effect was similarly attenuated by D-methionine administered either before or after noise exposure. Conclusion D-methionine administered before or after noise exposure could rescue NIHL by protecting cochlear morphology, inhibiting apoptosis, and maintaining connexin 26 and 30 expression.
机译:目的研究D-蛋氨酸在小鼠噪声性听力损失(NIHL)模型中的作用。方法我们调查了NIHL小鼠模型中听觉功能和耳蜗显微结构的变化,并进行了4-羟基壬烯(4-HNE)免疫染色和末端脱氧核苷酸转移酶dUTP缺口末端标记,并通过连接蛋白检测了连接蛋白26和30的表达水平。免疫印迹。结果噪声暴露可明显提高听觉脑干反应阈值。噪声暴露也损害了耳蜗基膜的内部毛发细胞,特别是外部毛细胞,而组织化学表明,在噪声暴露之前或之后,仅接受D-蛋氨酸处理的小鼠的基底膜中的毛细胞只有分散的损失。 D-蛋氨酸抑制耳蜗基底膜,血管纹和螺旋韧带的凋亡。噪声暴露增加了基底膜,血管纹和螺旋状副韧带中的4-HNE表达,但D-甲硫氨酸减弱了这种增加。噪声暴露会降低连接蛋白26和连接蛋白30的表达水平,并且在噪声暴露之前或之后施用D-甲硫氨酸同样会减弱这种作用。结论在噪声暴露之前或之后施用D-蛋氨酸可以保护耳蜗形态,抑制细胞凋亡并维持连接蛋白26和30的表达,从而挽救NIHL。

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