中文摘要：

目的分析铁必复颗粒对缺铁诱发肾虚耳聋大鼠耳蜗基底膜蛋白质表达的影响。方法健康幼龄Wistar大鼠随机分为两组。正常对照组大鼠喂以标准饲料16周；缺铁大鼠组采用缺铁饲料喂养8周，到至少有一耳ABRI阂值改变≥15dB时，再将这些模型大鼠随机分为肾虚耳聋组、铁必复颗粒治疗组。肾虚耳聋模型组继续喂以缺铁饲料8周，铁必复颗粒治疗组喂以添加铁必复颗粒的缺铁饲料8周。然后取大鼠耳蜗膜性组织进行蛋白质组学分析，比较差异表达蛋白质。结果正常对照组、肾虚耳聋组、铁必复颗粒治疗组分别检出989、1019、873组（个）蛋白质。与正常组和模型组组比较，铁必复颗粒治疗组耳蜗组织肌动蛋白、肌球蛋白、细胞骨架蛋白呈现高表达，并存在特异性高表达的46kDa、48kDa等尚未命名蛋白。结论铁必复颗粒可能通过调控相关特异性蛋白的表达水平，而参与肾虚耳聋模型大鼠耳蜗结构及功能的修复。

英文摘要：

Objective To investigate the effects of Tiebifu Granule on protein expression in the cochlea of rats with sensorineural hearing loss （SNHL） at the pattern of Kidney deficiency induced by iron insufficiency based on an experimental study. Methods Healthy young Wistar rats were randomly divided into two groups, with 20 in normal controlling group （NCG） and 100 in modelling group （MG）. The rats of NCG were fed with normal dietary for 16 weeks, and those in MG were fed with iron insufficiency diet for 8 weeks to prepare the model of iron insufficiency hearing loss, in which ABR threshold should be raised to the level ≥ 15 dB at least in one ear. Then, these modeled mrs were randomly divided into 2 sub-groups, i.e. deafness model group （DMG） at the pattern of Kidney deficiency, fed still with the same kind of diet being iron insufficient for another 8 weeks, and Tiebifu Granule treating group （TGTG）, fed with iron insufficient diet plus Tiebifu Granule for 8 weeks. By the end of experimental period, all the animals were put into death and membrane tissues of cochlea were taken from them to analyze the expressive differences of proteins in it by pmteomic profile technology. Results Protein dots determined by 2-DE from cochlear membrane samples were 989, 1019 and 873 for NCG, DMG and TGTG respectively. When compared with that of NCG and DMG, up-regulated were Actin, aortic smooth muscle, Actin, cytoplasmic 1, and Isoform 1 of Titin in thee tissue samples of TGTG, as well as other specifically up-regulated unnamed new proteins such as 46 kDa protein, 48 kDa protein and some others. Conclusions The therapeutic effect of Tiebifu Granule on sensorineural hearing loss may be brought about by regulating the expressive level of proteins specifically associated with structure and function reparation m cochlea as proven in this study among rats with heating loss at the pattern of Kidney deficiency.