线粒体在铝致神经细胞凋亡中的调控作用

目的探讨线粒体在铝致神经细胞凋亡中的调控作用。方法体外培养出生后0-3 d大鼠神经细胞,并用不同浓度氯化铝染毒,光学显微镜和电镜下观察神经细胞的凋亡现象及线粒体的形态学改变,并检测线粒体酶和凋亡相关蛋白的含量。结果光学显微镜及电镜下可以见到凋亡细胞的特征性改变,线粒体在电镜下肿胀变形并有结构的改变。线粒体酶在染毒低浓度组有代偿性活力升高,但中、高浓度组酶的活力仍然下降,高浓度组各酶活力显著低于对照组(P<0.01)。凋亡相关蛋白Caspase的含量随染毒浓度的增加而增多,且与染毒浓度有显著相关(P<0.01,r为0.963,0.859)。细胞色素C(CytC)在染毒组从线粒体释放至胞浆,3个染毒组间CytC的含量比较,差异无统计学意义(P>0.05)。结论线粒体的结构和酶活力的改变及其释放的促凋亡因子在铝致神经细胞凋亡的过程中起着重要的作用。

Role of Mitochondria in Al-induced Neurocyte Apoptosis

Objective To explore the role of mitochondria in Al-induced neurons apoptosis.Methods Neurons from 0~3 day newborn rats were cultured and treated with different concentration of aluminum chloride.Morphologic changes of neurons apoptosis and mitochondria were observed under light microscope and transmission electron microscope.Results Typical apoptosis morphologic characteristics of neurons were confirmed under light microscope and transmission electron microscope,and mitochondria were found swelling.The vitality of mitochondria enzyme in low dose group was found increased,but decreased in middle and high dose groups;the difference between high dose and control groups was significant.Active caspase-3 contents increased significantly in both cytoplasm and mitochondria as the aluminum concentration rose(P<0.01,r=0.963,0.859).CytC,which is localized only in mitochondria,was confirmed to be released into cytoplasm after aluminum treatment.The difference of CytC contents in 3 exposed groups was not significant.Conclusions Mitochondria structure and enzyme vitality changes,and its releasing apoptosis protein are all play important roles in Al-induced neurons apoptosis.