天麻素对甲基苯丙胺诱导的神经元毒性损害的保护作用

目的以褪黑素(melatonin,MT)为阳性对照,研究天麻素(gastrodin,GAS)对褪黑素(melatonin,MT)诱导的皮质神经元毒性损害的保护作用。方法(1)以不同浓度梯度MA(methamphetamine,MA)处理细胞24 h,检测细胞活力值,确定MA最佳给药浓度;再分别以不同浓度GAS、MT提前2 h干预并确定最佳干预浓度。(2)将细胞随机分为对照组、MA组、GAS+MA组和MT+MA组,每组细胞3个复孔,TUNEL法检测凋亡率。(3)免疫荧光检测Caspase-3的表达。结果(1)MA的最佳给药浓度为0.5 mmol·L^-1;MA处理后皮质神经元有胞体变小、突触变细,胞体空泡化等形态学变化;(2)GAS和MT的最佳干预浓度分别为25 mg·L^-1,10μmol·L^-1;(3)GAS预先干预可以降低MA引起的细胞凋亡,减弱Caspase3的表达,与MT的干预作用效果比较无明显差异。结论MA对皮质神经元有毒性损害作用,导致细胞凋亡;GAS干预可缓解MA介导的神经元毒性损害,缓解凋亡,其保护作用与MT相当。

The protective effects of gastrodin on methamphetamine-induced neurotoxicity

Aim To compare the protective effects of gastrodin and melatonin on methamphetamine(MA)-induced neurotoxicity of cortical neurons.Methods Cortical neuron cells were treated with different concentrations of methamphetamine for 24 h,then the cell viability was detected by CCK-8 kit to choose the optimal concentration of MA.The cells were treated with different concentrations of gastrodin or melatonin 2 h before the treatment of cells with optimal concentration of MA for 24 h.The optimal concentrations of gastrodin and melatonin were determined by CCK-8 kit as well.Cortical neuron cells were randomly divided into control group,MA group,gastrodin plus MA group,and melatonin plus MA group.Then the apoptotic rate of cells was detected by TUNEL method.The expression of Caspase-3 in cells was assessed by immunofluorescence.Results The optimal concentration of MA was 0.5 mmol·L^-1.After treating with MA,the numbers of cortical neurons decreased,the length of synapses became shorter,and the cell vacuolation,the number of dead cells increased.The optimal concentration of gastrodin was 25 mg·L^-1,and the optimal concentration of melatonin was 10μmol·L^-1.Gastrodin treat-ment could reduce the apoptosis of cortical neurons induced by MA,and the expression of Caspase-3 decreased as well,and there was no significant difference compared with the intervention effect of gastrodin with melatonin.Conclusions MA has neurotoxic damage to cortical neurons.Gastrodin could attenuate MA-induced neurotoxicity via alleviating the apoptosis induced by MA.