中文摘要：

[目的]研究钙稳态在邻苯二甲酸二丁酯（DBP）诱导大鼠皮层神经元凋亡中的作用。[方法]取胚胎大鼠皮层神经元,用25、50、100 mg/L的DBP进行细胞染毒,同时用加入10μmol/L钙络合剂（BAPTA-AM）和上述各浓度的DBP进行细胞培养,检测各组细胞的凋亡率、细胞内钙浓度（Fluo-3/AM荧光强度）、活性氧浓度以及线粒体膜电位。[结果]25、50、100 mg/L DBP染毒组的神经元凋亡率[（12.27±0.93）%、（18.53±0.87）%、（27.63±1.06）%],荧光强度[（10 623±826）%、（14 815±732）%、（18 328±708）%],细胞内活性氧的发生率[（10.21±1.05）%、（29.23±1.35）%、（34.68±1.03）%]及神经元线粒体膜电位下降率[（30.71±1.81）%、（45.30±3.25）%、（53.00±4.29）%]均高于对照组,差异均有统计学意义（P〈0.05）。随着DBP染毒剂量的增加,上述各项指标均呈剂量-效应关系（r=0.977,r=0.970,r=0.962,r=0.914,均P〈0.05）;BAPTA-AM干预后,与DBP同剂量组比较皮层神经元凋亡率有所降低,荧光强度明显下降,线粒体膜电位下降率降低,细胞内活性氧的发生率降低（均P〈0.05）。[结论]DBP可诱导大鼠皮层神经元凋亡,钙络合剂通过降低钙离子浓度,缓解DBP诱导的皮神经元的凋亡,表明钙稳态失衡促进DBP诱导的大鼠皮层神经元凋亡。

英文摘要：

[Objective] To study the role of calcium homeostasis in the apoptosis of rat cortical neurons induced by dibutylphthalate（DBP）.[Methods] Neurons were sampled from the cortex of pregnant rats.The cortical neurons were treated with 25,50,and 100 mg/L DBP;meanwhile,10 μmol/L calcium chelator（BAPTA-AM） was added into the above combinations.The apoptosis rates,intracellular free calcium concentrations [Ca2＋]i,reactive oxygen species（ROS）,and mitochondrial membrane potential of the cortical neurons were detected by flow cytometry.[Results] After treated with 25,50,and 100 mg/L DBP,the apoptosis rate [（12.27±0.93）%,（18.53±0.87）%,and（27.63±1.06）%,respectively],Fluo-3/AM fluorescence intensity [（10 623±826）%,（14 815±732）%,and（18 328±708）%],level of ROS [（10.21±1.05）%,（29.23±1.35）%,and（34.68±1.03）%],and decrease rate of mitochondrial membrane potential [（30.71±1.81）%,（45.30±3.25）%,and（53.00±4.29）%] were all higher than those of the control group（all Ps 〈 0.05） in a dose-response manner（r=0.977,r=0.970,r=0.962,r=0.914,all Ps 〈 0.05）.After treated with BAPTAAM,the apoptosis rates,Fluo-3/AM fluorescence intensity,level of ROS,and decrease rate of mitochondrial membrane potential of the cortical neurons were decreased compared with corresponding DBP only groups（all Ps 〈 0.05）.[Conclusion] DBP could induce rat cortical neuron apoptosis,and BAPTA-AM could blunt the apoptosis through decreasing [Ca2＋]i,suggesting that the disequilibrium of calcium homeostasis might promote the apoptosis of rat cortical neurons induced by BBP.