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目的：研究自噬在高压氧预处理预防脊髓缺血再灌注损伤中的机制。方法：新生大鼠脊髓神经元原代培养，分为对照组（氧糖剥夺）和高压氧（HBO）预处理组。通过应用免疫组织化学、Western blot分析两组LC3-Ⅱ与凋亡相关分子Beclin-1，Bcl-2，Caspase- 3的表达变化。结果：发现重复高压氧预处理对氧糖剥夺诱导原代培养的脊髓神经元损伤具有明显的保护作用。免疫组化和 Western blot显示与对照组相比高压氧预处理显著增加脊髓神经元细胞Bcl-2 的表达，降低Beclin-1，Caspase-3 以及自噬的特异性标记蛋白LC3-Ⅱ的表达。氧糖剥夺后对照组与高压氧组相比，LDH释放量明显增多(P<0.05)。结论：HBO预处理通过调节自噬减轻缺血再灌注损伤，为HBO预处理神经保护提供一条新的作用机制。

英文摘要:

Objective: To investigate the mechanism of autophagy in the hyperbaric oxygen pretreatment to prevent spinal cord ischemia-reperfusion injury. Methods: Neonatal rat spinal cord neurons were cultured. The neurons were divided into two groups: OGD (oxygen and glucose deprivation) and hyperbaric oxygen preconditioning (HBO) group. By the immunohistochemistry, Western blot analysis of two groups of Beclin-1, PI3K and apoptosis related molecules Bcl-2, of Beclin-1, LC3. Caspase-3 expression changes. Results: Repeated hyperbaric oxygen preconditioning on oxygen and glucose deprivation induced primary cultured spinal cord injury has a significant protective effect. Immunohistochemistry and Western blot showed that pretreatment with hyperbaric oxygenation compared with the control group significantly increase spinal cord neurons of Bcl-2 expression, reducing of Beclin-1, caspase-3 and the autophagy-specific marker protein LC3.-II's expression. Control group after oxygen and glucose deprivation compared with the HBO group, the LDH release was significantly increased (P<0.05). Conclusion: HBO pretreatment by regulating autophagy reduce the ischemic reperfusion injury, at the same time provide a novel mechanism of neuroprotection of HBO pretreatment.

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