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Change in gene expression in facial nerve nuclei and the effect of superoxide dismutase in a rat model of ischemic facial paralysis.

机译:大鼠缺血性面瘫模型中面神经核基因表达的变化和超氧化物歧化酶的影响。

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Peripheral nerve injury induces changes in gene expressions of a variety of neuroactive substances in cell somata, which may have roles in the adaptive response to the injury, neuronal survival, growth and regeneration. In this study, we designed a rat model of ischemic peripheral facial paralysis with a selective embolization technique, and observed mRNA expression of calcitonin gene-related peptide (CGRP), c-jun, and growth associated protein (GAP)-43 in facial nerve nuclei using in situ hybridization histochemistry. The rats were demonstrated to have a transient facial paralysis consistently, and thus this method was regarded as a model of minor peripheral nerve injury. The mRNA of CGRP, c-jun and GAP-43 showed a distinct pattern of induction and time course of increase after the ischemic nerve injury. The results suggest that the small injury to the peripheral nerve was able to induce changes in mRNA expression in the cell body of motoneurons. We also investigated the protective effect of superoxide dismutase (SOD), which is a free radical-scavenging enzyme involved in cellular antioxidant defenses. The SOD treatment clearly alleviated the behavioral impairment and decreased the CGRP mRNA expression at 3rd day after injury. These data suggest that a free radical generated by the ischemia may be partially responsible for ischemic nerve damage and the change in gene expression in motoneurons.
机译:周围神经损伤诱导细胞躯体中多种神经活性物质基因表达的变化,这可能在对损伤,神经元存活,生长和再生的适应性反应中起作用。在这项研究中,我们采用选择性栓塞技术设计了大鼠缺血性周围性面瘫的模型,并观察了降钙素基因相关肽(CGRP),c-jun和生长相关蛋白(GAP)-43在面部神经中的mRNA表达细胞核采用原位杂交组织化学。实验证明大鼠始终具有短暂的面神经麻痹,因此该方法被认为是轻度周围神经损伤的模型。缺血性神经损伤后,CGRP,c-jun和GAP-43的mRNA表现出明显的诱导方式和增加的时程。结果表明,周围神经的小损伤能够诱导运动神经元细胞体中mRNA表达的变化。我们还研究了超氧化物歧化酶(SOD)的保护作用,SOD是一种参与细胞抗氧化剂防御的自由基清除酶。 SOD处理可在受伤后第3天明显减轻行为障碍并降低CGRP mRNA表达。这些数据表明由缺血产生的自由基可能部分负责缺血神经损伤和运动神经元基因表达的变化。

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