耳聋左慈丸对老年肾虚耳聋小鼠耳蜗组织水通道蛋白4表达影响.docVIP

耳聋左慈丸对老年肾虚耳聋小鼠耳蜗组织水通道蛋白4表达影响.doc

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耳聋左慈丸对老年肾虚耳聋小鼠耳蜗组织水通道蛋白4表达影响

耳聋左慈丸对老年肾虚耳聋小鼠耳蜗组织水通道蛋白4表达影响   摘要:目的 观察耳聋左慈丸对老年肾虚耳聋小鼠耳蜗组织水通道蛋白4(AQP4)表达的影响,探讨其作用机制。方法 除正常组对照组外,其他小鼠采用腹腔注射氢化可的松方法复制肾虚小鼠模型,造模成功后,随机分为模型组、中药组,每组16只。中药组予耳聋左慈丸水煎液灌胃,模型组和正常对照组予生理盐水灌胃,共22 d。运用耳蜗铺片技术观察小鼠耳蜗内、外毛细胞与支持细胞的形态学变化;采用免疫组化法、Western blot检测耳蜗组织AQP4蛋白表达。结果 与正常对照组比较,模型组小鼠耳蜗内、外毛细胞和支持细胞缺失或散乱;与模型组比较,中药组耳蜗内、外毛细胞和支持细胞排列较整齐,边界尚清楚;小鼠耳蜗组织AQP4蛋白表达结果显示,与模型组比较,中药组AQP4蛋白表达增强(P0.01),中药组与正常对照组AQP4蛋白表达无显著差异。结论 耳聋左慈丸可能通过上调耳蜗组织AQP4蛋白表达,达到治疗肾虚小鼠耳聋的作用。   关键词:耳聋左慈丸;肾虚耳聋;耳蜗;水通道蛋白4;小鼠   DOI:10.3969/j.issn.1005-5304.2015.05.019   中图分类号:R285.5 文献标识码:A 文章编号:1005-5304(2015)05-0069-03   Abstract:Objective To investigate the effects of Erlong Zuoci Pills on AQP4 expression in cochlear tissue of mice with elderly kidney deficiency deafness;To discuss the action mechanism. Methods Intraperitoneal injection of hydrocortisone method was used to duplicate mice models with kidney deficiency except the normal control group. After the models were established, mice were divided into model group and TCM group, 16 mice in each group. TCM group was gavaged by Erlong Zuoci Pills, model group and normal control group were gavaged by normal saline for 22 d. Cochlear stretched preparation technology was used to observe morphological changes in cochlear inner and outer hair cells, and supporting cells. Immunohistochemistry and Western bolt were used to detect protein expression of AQP4. Results Compared with normal control group, mice in model group missed inner and outer hair cells and supporting cells of the cochlea. Compared with model group, arrangement of cochlear inner and outer hair cells and supporting cells was neat and boundary was clear in TCM group. Compared with model group, protein expression of AQP4 in cochlear tissues in TCM group increased (P0.01). There was no difference between TCM group and normal control group. Conclusion Erlong Zuoci Pills have significant therapeutic effect for elderly kidney deficiency deafness, and the treatment is related to the upregulation of protein expression of

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