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目的:探讨黄酮类化合物木犀草素对缺血/再灌损伤神经元的作用以及可能的作用机制。方法:原代培养的海马神经元经2 h的氧糖剥夺和24 h的再灌处理,分别检测细胞活性,乳酸脱氢酶漏出率和细胞凋亡率,采用Pu lsinelli四动脉阻断法对SD大鼠施行10 m in全脑缺血和24 h再灌,检测钠泵活性。结果:经氧糖剥夺/再灌后,海马神经元的活性比未经氧糖剥夺/再灌组显著地降低,乳酸脱氢酶漏出率和细胞凋亡率均显著地增高。在氧糖剥夺期间给予的木犀草素,在10~100μmol.L-1能呈剂量依赖地逆转这些改变。进一步实验发现木犀草素能够显著地增强大鼠全脑缺血/再灌后的钠泵活性。在神经元氧糖剥夺/再灌模型上,利用钠泵抑制剂哇巴因能阻断木犀草素的神经元保护作用。结论:木犀草素能减轻缺血/再灌所致的神经元损伤,其保护机制可能与增强了神经元细胞膜上的钠泵活性有关。
Objective: To investigate the effect of flavonoids luteolin on neurons in ischemia / reperfusion injury and its possible mechanism. Methods: Primary cultured hippocampal neurons were assayed for cell viability, lactate dehydrogenase leakage rate and apoptosis rate by 2 h oxygen sugar deprivation and 24 h reperfusion. Pu lsinelli four-artery occlusion SD rats were subjected to 10 min global cerebral ischemia and 24 h reperfusion, and sodium pump activity was measured. Results: After oxygen deprivation / reperfusion, the activity of hippocampal neurons was significantly lower than that without oxygen deprivation / reperfusion, the lactate dehydrogenase leakage rate and apoptosis rate were significantly increased. Luteolin, administered during oxy-glucose deprivation, reversed these changes in a dose-dependent manner at 10-100 μmol·L -1. Further experiments found that luteolin can significantly enhance the rat global cerebral ischemia / reperfusion after the sodium pump activity. On the neuronal oxytocosection / reperfusion model, ouabain, a sodium pump inhibitor, blocks neuronal protection of luteolin. CONCLUSION: Luteolin can relieve the neuronal damage induced by ischemia / reperfusion, and its protective mechanism may be related to the enhancement of sodium pump activity on neuronal cell membrane.