ABSTRACT
Traumatic optic nerve injury ( TON) is caused by direct or indirect optic nerve trauma, which is one of a serious complication of craniocerebral trauma. lts prognosis poor and usually bring permanent vision damage. At present, optic nerve injury and regeneration is hot in neurobiology research. To build an ideal experimental animal model is extremely important in research and development in the treatment of optic nerve injury. ln this article, we review the methods of making rat models of traumatic optic neuropathy, clinical similarities, advantages and disadvantages of among these models, to provide reference for more experimental study.
ABSTRACT
Objective Previous study showed that the histopathological basis of visual function damage caused by optical nerve injury is apoptosis of retinal ganglion cells(RGCs). This procedure is regulated by P53, bax and caspase 3 genes. Present study aimed to observe the expression of bax, P53 and caspase 3 mRNA in RGCs after traumatic optic nerve damage in the rats by SYBR green I fluorescence quantitative PCR method. Methods The animal model of optic nerve injury was established in the right eyes of 56 adult Wistar rats by a fluid percussion brain injury device (FPI) . Animal were killed on days 1, 3, 5, 7, 9, 14, 28 days separately after injury. Other 16 Wistar rats were divided into normal control group and sham operation group. The total RNA was isolated from rat fresh retina tissue by Trizol method and was treated by reverse transcription to cDNA using 01igo(dt) 18 as primer and then amplified. The target fragments of bax, P53 and caspase 3 cDNA were linked with carrier pTZ57 R/T to construct recombined plasmids which were transformated to E. Coli DH5α by T/A clone method. Recombined plasmids were extracted with alkaline lysis method and the plasmids were selected in white colonies by ampicillin screening, EcoR I restrictive enzyme analysis, and their specificity was evaluated using DNA sequencing. The standard curves were created by plasmid DNA and the precise expression level of target genes in samples were determined using software. The results were expressed as the ratios of target gene mRNA to GAPDH mRNA. Results The standard curve drawn by pTZ57R/T and target gene presented a good linear tendency with the higher sensitivity and specificity. The expression of P53 and bax mRNA began to increase on the third day after the injury of optic nerve and peaked on the fifth day and started to decline on the seventh day. The expression of caspase 3 mRNA increased from the fifth day through the ninth days after injury and declined on the fourteenth day. The significant differences were found in the expression of P53, bax and caspase 3 between model group and control group (P ＜ 0. 05) . Conclusion The pro-apoptotic protein P53, bax and caspase 3 play an important role in RGCs apoptosis.
ABSTRACT
PURPOSE: To evaluate the effect of high dose corticosteroid and optic canal decompression on the traumatic optic nerve injury. METHODS: Twenty six patients who were diagnosed to have traumatic optic nerve injury, were divided into two groups in which one group received corticosteroid therapy while the other group underwent optic canal decompression combined with corticosteroid therapy. RESULTS: Visual acuity increased by > OR =3 lines of LogMAR scale in 47% of the corticosteroid group, in 28% of operation and steroid group, and in 42% of overall cases. But the degree of visual acuity improvement had no difference between two groups(p=0.72). As the patients were divided into two groups based on initial visual acuity such as no light perception and light perception or better, the initial visual acuity did not have influence on the final visual outcome in both corticosteroid group and operation and steroid group(p=0.78, p=0.33). CONCLUSIONS: This result suggest that effect of high dose corticosteroid and optic canal decompression on traumatic optic nerve injury is not different.