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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,Casp-ase-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。
AIM: To investigate the mechanism of autophagy in the prevention of spinal cord ischemia-reperfusion injury by hyperbaric oxygen pretreatment. Methods: Primary cultured neonatal rat spinal cord neurons were divided into control group (oxygen deprivation) and hyperbaric oxygen (HBO) pretreatment group. The expression of LC3-Ⅱ and Beclin-1, Bcl-2 and Casp-ase-3 in two groups were detected by immunohistochemistry and Western blot. Results: It was found that repeated hyperbaric oxygen preconditioning had obvious protective effect on primary cultured spinal cord neurons induced by oxygen glucose deprivation. The results of immunohistochemistry and Western blot showed that hyperbaric oxygen pretreatment significantly increased the expression of Bcl-2 and decreased the expression of Beclin-1, Caspase-3 and autophagy-specific marker protein LC3-Ⅱ compared with the control group. Compared with hyperbaric oxygen group, the release of LDH in the control group was significantly increased after OGD (P <0.05). Conclusion: HBO preconditioning can relieve ischemia-reperfusion injury by regulating autophagy, providing a new mechanism of neuroprotection by HBO preconditioning.