Kong Xiangmei, Sun Xinghuai, Zhang Jinjun
Department of Ophthalmology, Eye Ear Nose and Throat Hospital, Medical Center of Fudan University, Shanghai 200031, China.
Yan Ke Xue Bao. 2004 Sep;20(3):171-7.
To evaluate the potential for Mecobalamin as a neuroprotective agent in optic nerve crush injury.
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 VitaminB12 or Mecobalamin (10 microg) 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.
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 VitaminB12-treated group (P = 0.037 and 0.035 respectively). More significantly, there were newly formed axons found in the Mecobalamin-treated group.
Optic nerve crush injury in rats causes the loss of the axons and RGCs but this may be ameliorated by treatment with Mecobalamin.
评估甲钴胺作为视神经挤压伤神经保护剂的潜力。
将24只成年Sprague-Dawley大鼠随机分为四组。一组作为正常对照组，另外三组大鼠的右眼接受视神经挤压伤。在三个挤压伤组中，一组不接受治疗，另外两组在挤压伤后立即肌肉注射维生素B12或甲钴胺（10微克），然后每两天注射一次。治疗一个月后处死所有大鼠，取出连有视神经的眼睛进行组织学检查。在光学显微镜（LM）和透射电子显微镜（TEM）下评估视神经轴突和视网膜神经节细胞（RGCs）的形态变化。计数轴突和RGCs的数量。
在本研究中，我们证明了甲钴胺作为视神经挤压伤后神经保护剂的潜力。我们发现，挤压伤后视神经轴突结构松散或遭到破坏。RGCs的线粒体肿胀，尼氏体不明显。此外，轴突和RGCs的数量显著减少（P<0.001）。然而，甲钴胺治疗后这些变化不那么明显。与未治疗的损伤组相比，该组保留了更多的轴突和RGCs（分别为P=0.010和0.003），与维生素B12治疗组相比也是如此（分别为P=0.037和0.035）。更显著的是，在甲钴胺治疗组中发现了新形成的轴突。
大鼠视神经挤压伤会导致轴突和RGCs丢失，但甲钴胺治疗可能会改善这种情况。
