人参二醇对β-淀粉样蛋白介导原代培养胎鼠皮质神经元毒性的保护作用

Protective Effects of Panoxadiol on Toxic of Amyloid β_(1-40) on Primary Cultured Fetal Rat Cortical Neuron

目的研究β-淀粉样蛋白(Aβ)1-40对原代培养胎鼠皮质神经元的毒性作用及人参二醇对Aβ1-40毒性的拮抗作用。方法通过测定原代培养胎鼠皮质神经元培养液中LDH的活力变化,并用四甲基偶氮唑蓝(MTT)法测定神经元存活率,观察Aβ1-40对神经元的毒性及人参二醇对神经细胞的保护作用。结果终浓度为3、6、12μmol/LAβ1-40作用于皮质神经元48h后,培养液中LDH的活力增高,神经细胞的存活率下降,与不作任何处理的空白对照组比较差异有显著性(P<0.05,P<0.01);与单独加入12μmol/LAβ1-40损伤组相比,经10、20、40mg/L人参二醇预处理24h再加入12μmol/LAβ1-40作用48h,LDH活力下降,细胞存活率升高,与仅加入12μmol/LAβ1-40的损伤组比较有统计学差异(P<0.05,P<0.01)。结论人参二醇能拮抗Aβ1-40诱导的神经细胞凋亡,对Aβ1-40引起的神经细胞毒性有一定保护作用。

Objective To investigate protective effects of panoxadiol on toxic of β-amyloid protein（ Aβ1-40 ） on primary cultured fetal rat cortical neuron and to explore antagonism of panoxadiol to toxicity of Aβ1-40. Methods Changes of vitality of lactate dehydrogenase（LDH） in culture solution Of primary cultured fetal rat cortical neuron were detected. Survival rate was detected with methyl thiazolyl tetrazolium（MTF） and injury of Aβ1-40 on neuron and protection of panoxadiol. Results LDH activity increased and survival rate of nerve cells decreased in culture so- lution after cortical neuron performed with Aβ1-40 （3,6 and 12μmol/L）for 48 hours, which was obviously different from that in control group （P 〈0.05, 〈0.01 ） ;LDH activity decreased and survival rate of nerve ceils increased in group of pretreatment with panoxadiol for 24 hours fol- lowed by addition of 12μmol/L Aβ1-40 for 48 hours, which was significant difference compared with group performed with single 12μmol/L Aβ1-40 The indices of group of pretreatment of 10 mg/L panoxadiol and 40mg/L panoxadiol were significant difference from those of injured group（P 〈 0.05, 〈 0.01 ）. Conclusion Panoxadiol can play a very important role＇in inhibiting apoptosis of nerve cells induced by Aβ1-40 and serve as an certain protection on cytotoxicity of nerve cells induced by Aβ1-40.