原创力文档早期高压氧治疗对颅脑损伤神经细胞凋亡的影响（Effect of early hyperbaric oxygen therapy on neuronal apoptosis in traumatic brain injury）精选.doc
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早期高压氧治疗对颅脑损伤神经细胞凋亡的影响（Effect of early hyperbaric oxygen therapy on neuronal apoptosis in traumatic brain injury）精选
早期高压氧治疗对颅脑损伤神经细胞凋亡的影响（Effect of early hyperbaric oxygen therapy on neuronal apoptosis in traumatic brain injury）
Effect of early hyperbaric oxygen therapy on neuronal apoptosis in traumatic brain injury
This article source: paper /
Authors: Liu Yong, Chen Xianglin, Zhu Yufu, Yan Jingfeng, Kong Lingsheng, Feng Jun, Hu Xiaobing
[Abstract] Objective To study the effect of early hyperbaric oxygen therapy on the expression of related genes Bcl-2 and Bax after traumatic brain injury in rats, and to investigate the early protective effects of hyperbaric oxygen therapy on the injured neurons. Methods 100 SD rats of clean grade were randomly divided into normal group (nor), 20 trauma group (TBI), 40 hyperbaric oxygen treatment group (HBOT), 40 rats. Using Allen s modified method, the model of free fall brain injury in rats was established, and hyperbaric oxygen therapy was performed within 6 h after injury. 8 h after injury and 1, 3, 5, 8 days were animal drawn, hematoxylin eosin staining to observe the morphological changes of cells, each cell apoptosis detection rate observed by flow cytometry, immunohistochemistry, expression of Bcl-2 Bax protein in cortex and hippocampus cells in the detection method. Results in HBOT group, the cortex and hippocampus cells of the TBI group were all morphologically regular and arranged more regularly than those in group B, and there were many levels of nucleus staining and pyknosis. Compared with group TBI, the apoptosis rate of HBOT group decreased significantly at each time point (p 0.05). The expression intensity of Bcl-2 in each phase of HBOT group was higher than that in group TBI (P 0.05, p 0.01), and the expression intensity of Bax was significantly lower than that of group TBI (P 0.01). Conclusion early hyperbaric oxygen therapy can obviously promote the high expression of Bcl-2 and inhibit the expression of Bax, which can effectively inhibit the apoptosis after traumatic brain injury.
[Keywords] brain damage; early stage; hyper
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