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为了探讨噪声暴露对豚鼠血迷路屏障通透性的影响及ERK1/2磷酸化在此过程中的作用,本文将豚鼠随机分为噪声暴露组和对照组;暴露组又分为两组,暴露时间分别为4 h和6 h。然后用Evans蓝染色和硝酸镧示踪法检测血迷路屏障的通透性,Western blot方法检验耳蜗组织中ERK1/2及其磷酸化蛋白的表达。结果显示:噪声暴露后4 h和6 h,耳蜗组织Evans蓝的染色强度均显著高于对照组(P<0.05);对照组镧颗粒仅滞留在血管纹毛细血管腔内,噪声暴露组镧颗粒分别见于毛细血管腔、血管内皮细胞和血管周围组织内;另外,噪声暴露组(4 h和6 h)耳蜗组织ERK1/2水平与对照组接近,但ERK1/2的磷酸化程度明显增加;两种噪声暴露处理对豚鼠血迷路屏障通透性及ERK1/2磷酸化水平的影响存在明显的剂量依赖效应;ERK1/2抑制剂PD98059可部分降低血迷路屏障的通透性。以上结果提示噪声暴露可增加血迷路屏障的通透性,其机制可能是通过诱导ERK1/2磷酸化来实现的。
In order to investigate the effect of noise exposure on the permeability of guinea pig blood-labyrinth barrier and the role of ERK1 / 2 phosphorylation in this process, guinea pigs were randomly divided into noise exposure group and control group. The exposure group was divided into two groups. The exposure time Respectively 4 h and 6 h. The permeability of the blood-labyrinth barrier was detected by Evans blue staining and lanthanum nitrate tracing method. The expression of ERK1 / 2 and its phosphorylated protein in cochlea was detected by Western blot. The results showed that the staining intensities of Evans blue in cochlear tissues at 4 h and 6 h after noise exposure were significantly higher than those in the control group (P <0.05). The lanthanum particles in the control group only retained in the capillary vessels of the vasculature, and the lanthanum particles Respectively, in the capillary cavity, vascular endothelial cells and perivascular tissue. In addition, ERK1 / 2 levels in the cochlear of the noise-exposed group (4 h and 6 h) were similar to those in the control group, but the phosphorylation of ERK1 / 2 was significantly increased. There was a significant dose-dependent effect of noise exposure on the permeability of the blood-labyrinth barrier and phosphorylation of ERK1 / 2 in guinea pigs. PD98059, an inhibitor of ERK1 / 2, partially decreased the permeability of the blood-labyrinth barrier. The above results suggest that noise exposure may increase the permeability of the blood-labyrinth barrier, and its mechanism may be through the induction of ERK1 / 2 phosphorylation.