缝隙连接蛋白26和30在大鼠2型糖尿病性耳聋模型中的表达

Expression of connexin 26 and 30 in cochlea in a rat model of type 2 diabetes

目的探讨缝隙连接蛋白(Cx)26和Cx30在大鼠2型糖尿病耳蜗中的表达,及两者在2型糖尿病性耳聋发病机制中的作用。方法60只Wistar大鼠随机分为实验组(40只)和对照组(20只);实验组以腹腔注射10 mg/L链脲佐菌素建立2型糖尿病模型,检测模型成功前及成功后第1、2、3、4、5月的听性脑干反应(ABR),采用HE染色观察两组耳蜗形态变化;免疫荧光、Western blotting检测Cx26和Cx30在两组大鼠耳蜗的表达变化。结果实验组在模型成功后第1、2、3、4、5月Click-ABR 60dBSPLⅢ波、Ⅴ波潜伏期和Ⅰ~Ⅲ、Ⅰ~Ⅴ波间期较对照组延长(P<0.05);实验组螺旋韧带和螺旋神经节中细胞数量少于对照组(P<0.05);实验组Cx26和Cx30在成模后2、3、4、5月表达较对照组减少(P<0.05),且随着时间延长,两种蛋白表达逐渐降低。结论Cx26和Cx30在大鼠2型糖尿病模型耳蜗中表达减少,且与听力损害出现时间相同。

Objective To study the expression of connexin(Cx)26 and Cx30 in the cochlea in rat model of type 2 diabetes,and their role in the hearing loss of type 2 diabetes.Methods Sixty wistar rats were randomly divided into a control group(n=20)and a experimental group(n=40).Rats in the experimental group received intraperitoneally injection of 10 mg/L streptozotocin to establish model of type 2 diabetes.Auditory brainstem response(ABR)was tested before and after molding at month 1,2,3,4,5.The morphology of cochlea was observed by HE staining,and the level and pattern of Cx26 and Cx30 expression within the cochlea were detected by immunofluorescence and Western blotting.Results In rats in the diabetes group,waveⅢandⅤlatency,Ⅰ-ⅢandⅠ-Ⅴinterval of Click-ABRs(60 dBSPL)prolonged at month 1,2,3,4,5 after molding compared to the control(P<0.05).The number of cells was obvious reduced in the spiral ligament and ganglion of the experimental group(P<0.05).Immunofluorescence and Western blotting results showed decreased expression of Cx26 and Cx30 in the experimental group at 2,3,4,5 month(P<0.05),and the expression of the two proteins decreased gradually with the time extension.Conclusion Expression of Cx26 and Cx30 is reduced at the same time as the occurrence of hearing impairment in rat cochlea with type 2 diabetes.