羟丁酸钠对皮质神经元缺氧复氧损伤的保护作用(英文)

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。

Neuroprotective effects of sodium γ-hydroxybutyrate against cortical neuron injury induced by hypoxia-reoxygenation

AIM To understand the protective mechanism of sodium γ-hydroxybutyrate(GHB) on ischemic brain. METHODS Cultures of cortical neurons were subjected to hypoxia for 2 h followed by reoxygenation for 6 h. GHB(5, 20, 80 mmol*L-1) was added to the bath medium 30 min before hypoxia-reoxygenation. Neuron survival and lactate dehydrogenase (LDH) efflux in the bathing medium were assayed for the evaluation of neuronal injury. Malonyldialdehyde (MDA) content, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured using colorimetry. RESULTS Hypoxia-reoxygenation reduced survival rate of neurons, increased LDH efflux and MDA content, decreased SOD and GSH-Px activities. GHB 20, 80 mmol*L-1 increased the rate of survival neurons while reduced LDH efflux and MDA content. SOD and GSH-Px activities were significantly increased with GHB pretreatment. CONCLUSION GHB protects neurons against hypoxia-reoxygenation injury and this effect is related to its action on antioxidant enzymes.