Xiangmei Kong1, Xinghuai Sun, Jinjun Zhang. 1. Department of Ophthalmology, Eye Ear Nose and Throat Hospital, Medical Center of Fudan University, Shanghai 200031, China.
Abstract
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 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. 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 VitaminB12-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.
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 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. 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 VitaminB12-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.