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目的 研究羟丁酸钠 (GHB)对缺氧复氧脑损伤的保护机制。方法 用原代培养大鼠皮层神经元建立缺氧复氧损伤模型 ,缺氧 2h复氧 6h ;缺氧前30min在培养基内加入GHB(5 ,2 0 ,80mmol·L- 1) ,观察神经元的形态学变化 ,检测培养基中乳酸脱氢酶漏出率及细胞中丙二醛 (MDA)含量、超氧化物歧化酶 (SOD)和谷胱甘肽过氧化物酶 (GSH Px)的活力。结果 缺氧复氧降低神经元生存率 ,增加乳酸脱氢酶 (LDH)漏出及MDA含量 ,而导致SOD及GSH Px活力下降。GHB 2 0 ,80mmol·L- 1预处理能显著提高缺氧复氧神经元的生存率 ,减少LDH的漏出及MDA的生成 ,升高SOD和GSH Px的活力。结论 GHB对缺氧复氧引起的神经元损伤的保护作用与它保护抗氧化酶的作用有关。
Objective To study the protective mechanism of sodium oxybate (GHB) on hypoxic-reoxygenation brain injury. Methods Hypoxia / reoxygenation injury model was established by primary cultured rat cortical neurons. Hypoxia and reoxygenation was performed 6 h after hypoxia for 6 h. GHB (5, 20, 80 mmol·L- 1) was added to the medium 30 min before hypoxia. The changes of cell morphology, the leakage rate of lactate dehydrogenase (LDH) and the content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH Px) . Results Hypoxia and reoxygenation reduced the survival rate of neurons, increased the leakage of lactate dehydrogenase (LDH) and the content of MDA, which led to the decrease of the activity of SOD and GSH Px. Pretreatment with GHB20 and 80 mmol·L -1 significantly increased the survival rate of hypoxia-reoxygenation neurons, decreased the leakage of LDH and the production of MDA, and increased the activities of SOD and GSH Px. Conclusions The protective effects of GHB on neuronal injury induced by hypoxia and reoxygenation are related to the protective effect of GHB on the antioxidant enzymes.