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目的 :进一步探讨高压氧治疗脑缺血再灌注损伤 ,减轻神经元凋亡从而发挥保护作用的机理。方法 :采用“双侧颈总动脉阻断法”前脑缺血模型 ,对沙土鼠前脑缺血 2 0min后再灌注 3d ,并用 0 .15MPa和 0 .2 5MPa压力的高压氧治疗 (6 0min/d ,连续 3d)后 ,应用免疫组化LSAB方法 ,观察高压氧对海马CA1,区神经元凋亡相关基因bcl 2和bax的蛋白表达的影响。结果 :沙土鼠脑缺血再灌注 3d组海马CA1区大量神经元表达Bax蛋白 ,并且神经元发生凋亡 ,未见神经元表达Bcl 2蛋白 ;高压氧治疗组则大量神经元表达Bcl- 2蛋白 ,并且 0 .2 5MPa高压氧治疗组比0 .15MPa高压氧治疗组变化更显著 ,而各组表达Bax蛋白的神经元数目无明显变化 ,但高压氧治疗组Bax蛋白阳性的神经元形态正常。结论 :HBO暴露可诱导大量神经元表达Bcl- 2蛋白 ,对Bax蛋白表达则无明显作用 ,使Bcl 2和Bax蛋白表达的比值增高 ,从而起到保护神经元的作用 ,这可视为HBO治疗脑缺血性损伤减少神经元凋亡的机理之一
Objective: To further explore the mechanism of hyperbaric oxygen treatment of cerebral ischemia-reperfusion injury, reduce neuronal apoptosis and play a protective role. Methods: The forebrain ischemia models of bilateral common carotid artery occlusion were used to reperfuse the ischemic forebrain of the gerbils for 20 days and reperfused for 3 days. The rats were anesthetized with hyperbaric oxygen at 0,15 MPa and 0,25 MPa / d for 3days), immunohistochemistry LSAB method was used to observe the effect of hyperbaric oxygen on the protein expression of apoptosis-related genes bcl 2 and bax in hippocampal CA1 and neurons. Results: A large number of neurons in the hippocampal CA1 region of gerbil cerebral ischemia-reperfusion group 3 expressed Bcl-2 protein, and neurons were apoptotic. No neurons expressed Bcl2 protein. In hyperbaric oxygen group, a large number of neurons expressed Bcl- , And 0. 25MPa hyperbaric oxygen treatment group than 0. 15MPa hyperbaric oxygen treatment group more significant changes in the group of Bax protein expression in the number of neurons did not change significantly, but hyperbaric oxygen treatment group Bax protein positive neurons normal morphology. CONCLUSION: HBO exposure induces Bcl-2 protein expression in a large number of neurons and has no effect on the expression of Bax protein, thus increasing the ratio of Bcl-2 and Bax protein expression and thereby protecting neurons. This may be considered as HBO treatment One of the mechanisms of neuronal apoptosis induced by cerebral ischemic injury