摘要
目的观察一氧化氮合酶抑制剂1400W(N-(3-(氨甲基)-苄基)乙脒)对内毒素(endotoxin,ETX)所致的豚鼠血迷路屏障损伤的保护作用,并初步探讨其可能机制。方法将豚鼠分3组,每组分别于听泡内各注入无菌生理盐水、ETX和ETX加1400W,光镜观察耳蜗形态变化;以伊文思蓝(Evans Blue,EB)为示踪剂,测量EB通过耳蜗血迷路屏障的渗出量;用硝酸还原酶法检测各组耳蜗组织一氧化氮(NO)含量的变化。结果ETX组EB渗出量增加,同时有NO含量增加;ETX加1400W组和ETX组比较,EB渗出量减少(P<0.05),NO生成亦减少(P<0.05)。无菌生理盐水组无EB通过,亦无NO含量增加。结论ETX可能通过诱导NO生成而引起血迷路屏障通透性增加,此作用可以被1400W抑制,后者可能减轻中耳炎引起的内耳损害。
Objective To investigate the effects of 1400W on the endotoxin-induced alteration of permeability of blood-labyrinth barrier of guinea pigs and to explore its possible mechanisms. Methods Guinea pigs were divided into three groups. Sterile-physiological saline solution（control）, endotoxin, endotoxin plus 1400W were injected respectively into each tympanic cavity of the three groups of guinea pigs via superior bulla. Evans blue（EB） was injected via jugular vein before sacrification. Then, the pathological changes of the cochlea were examined by light microscopy. The EB that crossed the blood-labyrinth barrier and the amounts of NO in the cochlea were detected. Results The permeability of the blood-labyrinth barrier of the endotoxin plus 1400W group was significantly lower than that of the endotoxin group（P 〈 0.01）. Moreover, NO amounts in the endotoxin plus 1400W group were markedly lower than those in the endotoxin group （P 〈 0.05）. Conclusion Endotoxin might increase the permeability of blood-labyrinth barrier through induction of NO expression in the cochlea. Conversely, application of 1400W might attenuate the enhancement of permeability via downregulation of NO expression in the inner ear, raising the possibility of 1400W application as a potential approach to otitis media suppurativa-associated deafness prevention.
出处
《中华耳科学杂志》
CSCD
2008年第3期331-334,共4页
Chinese Journal of Otology
