摘要
目的探讨人参炔醇对原代神经细胞氧化应激的保护作用。方法通过MTT法、流式细胞术观察人参炔醇对神经细胞氧化应激的影响;并观察人参炔醇体外对自由基的清除作用及对细胞内超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性与丙二醛(MDA)含量的影响。结果2～16μmol/L人参炔醇对H2O2损伤神经细胞有一定的保护作用,可剂量依赖性地促进细胞存活,8μmol/L人参炔醇可显著减少细胞的坏死率及凋亡率(P<0.01)。30～100μmol/L人参炔醇对自由基有一定的清除作用,2～8μmol/L人参炔醇还可显著提高H2O2损伤细胞内SOD、GSH-Px活性并抑制MDA的生成(P<0.01)。结论人参炔醇具有保护神经细胞对抗氧化应激的活性,该活性与细胞内SOD活性增高有关。
Objective To investigate the neuroprotective effect of panaxynol on primary cultured cortical neuron against oxidative stress. Methods Viability of panaxynol acted on neuron oxidative stress was monitored by MTT assay and FCM method. Scavenging effects of panaxynol on free radicals were observed in vitro. Effects of panaxynol on SOD activity and GSH-Px, and MDA content in primary neuron injured by H_2O_2 were also determined. Results Panaxynol (2—16 μmol/L) could dose-dependently protect neuron from oxidative stress induced by H_2O_2; 8 μmol/L of panaxynol could decrease necrosis and apoptosis rate of neuron significantly (P<0.01). Panaxynol (30—100 μmol/L) could scavenge free radicals. Panaxynol (2—8 μmol/L) could significantly improve the activities of SOD and GSH-Px, and inhibit MDA formation (P<0.01) in primary cultured neuron injured by H_2O_2. Conclusion The protective effects of panaxynol on neuron against oxidative stress may be related with the increase of SOD activity in cytoplasm.
出处
《中草药》
CAS
CSCD
北大核心
2005年第1期72-75,共4页
Chinese Traditional and Herbal Drugs
基金
国家自然科学基金资助项目(30371731)
上海第二医科大学-上海交通大学联合科研基金资助项目(2003HZJJ002)
上海市教委学科建设专项基金部分资助(JY2001)
