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The Protective Role of Mecobalamin Following Optic Nerve Crush in Adult Rats

机译：甲钴胺对视神经粉碎后成年大鼠的保护作用

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Purpose: To evaluate the potential for Mecobalamin as a neuroprotective agent in optic nerve crush injury. Methods: Twenty-four adult Sprague-Dawley rats were randomly divided into four groups. One group acted as normal controls, while in the other three groups the right eye was subjected to optic nerve crush injury. Of the three crush injury groups one group received no treatment, while the other two groups received intramuscular injections of VitaminB_(12) or Mecobalamin (10 μg) immediately after crush injury and then every two days. All the rats were sacrificed one month post-treatment, and the eyes attached with optic nerves were removed for histology. The morphological changes of optic nerve axons and retinal ganglion cells (RGCs) were assessed under light microscope (LM) and transmission electromicroscope (TEM). The numbers of axons and RGCs were counted. Results: In this study we demonstrate the potential for Mecobalamin as a neuroprotective agent following optic nerve crush injury. We show here that the axons of optic nerves were loose in structure or destroyed. The mitochondria of the RGCs was swollen, and the Nissel body was less evident after the crush injury. Moreover, the number of axons and RGCs was significantly reduced (P< 0.001). However, these changes were less dramatic after the Mecobalamin-treatment. More axons and RGCs were remained in the group than those in the untreated injury group (P= 0.010 and 0.003 respectively), and those in the VitaminB_(12)-treated group (P =0.037 and 0.035 respectively). More significantly, there were newly formed axons found in the Mecobalamin-treated group. Conclusions: Optic nerve crush injury in rats causes the loss of the axons and RGCs but this may be ameliorated by treatment with Mecobalamin.
机译：目的：评估甲钴胺在视神经挤压伤中作为神经保护剂的潜力。方法：将24只成年Sprague-Dawley大鼠随机分为四组。一组作为正常对照，而在其他三组中，右眼遭受视神经挤压伤。在三个挤压伤组中，一组没有接受任何治疗，而其他两组在挤压伤后立即然后每两天肌肉注射一次维生素B_（12）或甲钴胺（10μg）。治疗后一个月将所有大鼠处死，并摘除附有视神经的眼睛以进行组织学检查。在光学显微镜（LM）和透射电镜（TEM）下评估视神经轴突和视网膜神经节细胞（RGC）的形态变化。计算轴突和RGC的数目。结果：在这项研究中，我们证明了甲钴胺在视神经挤压伤后作为神经保护剂的潜力。我们在这里表明视神经轴突的结构松散或被破坏。 RGC的线粒体肿胀，挤压伤后尼塞尔体不明显。此外，轴突和RGC的数量显着减少（P <0.001）。但是，在接受甲钴胺治疗后，这些变化不那么明显。与未经治疗的损伤组（分别为P = 0.010和0.003）和经过维生素B_（12）治疗的组（分别为P = 0.037和0.035）相比，该组中保留的轴突和RGC数量更多。更重要的是，在接受甲钴胺治疗的组中发现了新形成的轴突。结论：大鼠视神经挤压伤可引起轴突和RGC的损失，但通过甲钴胺治疗可减轻这种情况。

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