Sun Shujuan, Zhang Daogong, Sun Gaoying, Song Yongdong, Cai Jing, Fan Zhaomin, Wang Haibo
Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial ENT Hospital Affiliated to Shandong University , Jinan 250022 , P.R. China.
Acta Otolaryngol. 2019 Nov;139(11):966-976. doi: 10.1080/00016489.2019.1663365. Epub 2019 Sep 19.
To date, the pathogenesis of Meniere's disease (MD) remains unclear. Previous research found that the SLC4A1 gene significantly down-regulated. : This study sought to understand the effect of SLC4A1 on the pathogenesis of MD. ELH C57 mice models were induced by intraperitoneal injection of AVP. The mRNA expression levels of SLC4A1, SLC4A10 and SLC26A4 were monitored by real-time quantitative PCR, the protein expression levels of SLC4A1 were monitored by immunoblotting and immunofluorescence before and after the ELH. DIDS is an inhibitor of SLC4A1. The expression levels of SLC4A1 were also monitored in the AVP + DIDS group. We successfully established the model of ELH after applied AVP. The results of HE staining showed displacement of Reissner's membrane with bulge to scala vestibule in ears of the AVP group. Cochlea/ELS SLC4A1 protein and SLC4A1, SLC4A10, SLC26A4 mRNA expressions were reduced significantly in C57 mice of the AVP group. The SLC4A1 protein expression levels and SLC4A1, SLC4A10, SLC26A4 mRNA expression levels declined more obvious in the cochlea and ELS in C57 mice of the AVP + DIDS group. SLC4A1 was a protective factor in the pathogenesis of MD, but the mechanisms were unknown.
迄今为止，梅尼埃病（MD）的发病机制仍不清楚。先前的研究发现SLC4A1基因显著下调。本研究旨在了解SLC4A1对MD发病机制的影响。通过腹腔注射血管加压素（AVP）诱导ELH C57小鼠模型。在ELH前后，通过实时定量PCR监测SLC4A1、SLC4A10和SLC26A4的mRNA表达水平，通过免疫印迹和免疫荧光监测SLC4A1的蛋白表达水平。DIDS是SLC4A1的抑制剂。在AVP + DIDS组中也监测SLC4A1的表达水平。应用AVP后，我们成功建立了ELH模型。HE染色结果显示，AVP组小鼠耳内的Reissner膜移位并向前庭阶膨出。AVP组C57小鼠的耳蜗/内淋巴囊SLC4A1蛋白以及SLC4A1、SLC4A10、SLC26A4 mRNA表达显著降低。AVP + DIDS组C57小鼠耳蜗和内淋巴囊的SLC4A1蛋白表达水平以及SLC4A1、SLC4A10、SLC26A4 mRNA表达水平下降更为明显。SLC4A1是MD发病机制中的一个保护因子，但其机制尚不清楚。
