【摘要】：目的觀察長(zhǎng)期注射水楊酸鈉對(duì)大鼠聽(tīng)性腦干反應(yīng)(ABR)及下丘谷氨酸脫羧酶-67(GAD67)表達(dá)的影響。方法將18只成年健康Wistar大鼠隨機(jī)分為水楊酸鈉組、生理鹽水組、對(duì)照組,每組6只。水楊酸鈉組肌肉注射10%水楊酸鈉175mg/kg,2次/天,連續(xù)28天;生理鹽水組每天相同時(shí)間注射等量生理鹽水;對(duì)照組不注射任何藥物。造模結(jié)束后,使用美國(guó)TDT系統(tǒng)對(duì)三組大鼠進(jìn)行ABR反應(yīng)閾及波Ⅲ潛伏期檢測(cè),然后將大鼠斷頭處死并取腦,剝離下丘。采用蛋白質(zhì)印跡(Western blot)方法檢測(cè)下丘GAD67蛋白表達(dá)的變化。結(jié)果①水楊酸鈉組、生理鹽水組、對(duì)照組ABR反應(yīng)閾分別為61.67±4.08、33.33±2.58、35.83±2.04dB SPL,波Ⅲ潛伏期分別為3.97±0.28、3.51±0.11、3.52±0.09ms。水楊酸鈉組較生理鹽水組、對(duì)照組ABR反應(yīng)閾明顯升高,波Ⅲ潛伏期明顯延長(zhǎng)(P0.01),而生理鹽水組與對(duì)照組差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05);②水楊酸鈉組下丘GAD67蛋白表達(dá)水平明顯高于生理鹽水組、對(duì)照組(P0.01),而生理鹽水組與對(duì)照組下丘GAD67蛋白表達(dá)水平差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論長(zhǎng)期注射水楊酸鈉可導(dǎo)致大鼠下丘GAD67蛋白表達(dá)水平升高,GAD67蛋白表達(dá)的上調(diào)可能作為一種負(fù)反饋以代償去抑制所引起的興奮與抑制的失衡狀態(tài),促進(jìn)抑制性效應(yīng)的產(chǎn)生,該蛋白表達(dá)的改變極有可能作為機(jī)體對(duì)水楊酸鈉耳毒性的抑制性代償反應(yīng)和調(diào)節(jié)機(jī)制之一。
[Abstract]:Objective to observe the effect of sodium salicylate injection on the expression of (ABR) and glutamate decarboxylase 67 (GAD67) in rat auditory brainstem response. Methods 18 healthy adult Wistar rats were randomly divided into sodium salicylate group, normal saline group and control group with 6 rats in each group. Sodium salicylate group was intramuscularly injected with 10% sodium salicylate (175 mg / kg 路kg ~ (-1) twice a day for 28 days; saline group was injected with the same amount of saline at the same time every day; the control group was not injected with any drugs. The ABR response threshold and wave 鈪，

本文編號(hào)：2149141