亚氨乙基赖氨酸对庆大霉素所致豚鼠耳蜗损伤的拮抗作用

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探讨亚氨乙基赖氨酸对庆大霉素所致豚鼠耳蜗损伤的拮抗作用。将实验豚鼠分为正常对照组、实验对照组和实验组。实验对照组和实验组豚鼠皮下注射庆大霉素,同时实验组豚鼠腹腔注射亚氨乙基赖氨酸,实验对照组豚鼠腹腔注射等量生理盐水。正常对照组豚鼠皮下及腹腔均注射等量的生理盐水。用免疫组织化学的方法检测诱生型一氧化氮合成酶在各组豚鼠耳蜗中的表达。用ABR检测各组豚鼠听阈的改变,同时以扫描电镜观察耳蜗毛细胞的损伤。结果显示,诱生型一氧化氮合成酶在正常对照组耳蜗的表达呈阴性,在实验对照组和实验组耳蜗的表达呈阳性,且在实验对照组的表达强于实验组。实验组ABR阈移明显小于实验对照组,且实验组耳蜗的损伤明显轻于实验对照组。研究表明,诱生型一氧化氮合成酶在庆大霉素损伤耳蜗中呈阳性表达,亚氨乙基赖氨酸对庆大霉素所致豚鼠耳蜗损伤有明显的拮抗作用,提示一氧化氮在庆大霉素所致耳蜗的损伤中起重要作用。 To investigate the antagonistic effect of iminoethyllysine on cochlear damage induced by gentamicin in guinea pigs. Guinea pigs were divided into normal control group, experimental control group and experimental group. Experimental control group and experimental group guinea pigs were injected gentamicin subcutaneously, the experimental group guinea pig intraperitoneal injection of iminoethyl lysine, experimental control group guinea pigs were injected intraperitoneally with the same amount of saline. The normal control group of guinea pigs were injected subcutaneously and intraperitoneally with the same amount of normal saline. Immunohistochemistry was used to detect the expression of inducible nitric oxide synthase in cochlea of ​​each group. ABR was used to detect the change of hearing threshold of guinea pigs in each group, and the damage of cochlear hair cells was observed by scanning electron microscope. The results showed that the expression of inducible nitric oxide synthase in the normal control group was negative. The expression of cochlear in the experimental group and the experimental group was positive, and the expression in the experimental group was stronger than that in the experimental group. ABR threshold shift in the experimental group was significantly less than that of the experimental control group, and the cochlear injury of the experimental group was significantly lighter than that of the experimental control group. Studies have shown that inducible nitric oxide synthase positive expression in cochlea gentamicin injury, iminoethyl lysine gentamicin-induced guinea pig cochlear injury significantly antagonized, suggesting that nitric oxide Gentamicin-induced cochlear injury plays an important role.
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