不同浓度的5-氮杂胞苷对RPMI 8226细胞系的诱导凋亡作用分析

目的:探讨不同浓度的5-氮杂胞苷对RPMI 8226细胞系的诱导凋亡作用.方法:对RPMI 8226细胞系采用5-氮杂胞苷0μmol/L、2μmol/L、5μmol/L、10 μrnol/L、20 μmol/L、50 μmol/L处理24 h、48 h、72 h,并对RPMI 8226细胞系处理后进行刮痕实验,12h后对细胞迁移进行比较.结果:在作用24h、48h时,随着作用浓度的增加,RPMI-8226细胞的抑制率出现明显的增加,但在作用72 h时,我们发现10 μmol/L、20μmol/L、50μnol/L其对RPMI-8226细胞的抑制效果无明显的差异性;刮痕实验后12h后其出现差异性,其中药物浓度越大其对RPMI-8226细胞的运动迁移能力越弱.结论:DNA甲基化转移酶抑制剂5-氮杂胞苷可对RPMI-8226细胞的凋亡具有良好的诱导效果,同时可抑制RPMI-8226细胞的增殖以及迁移.     

甘草次酸抑制骨肉瘤细胞MG63增殖的NF-κB信号通路机制*

目的: 探讨甘草次酸抑制骨肉瘤细胞MG63增殖的机制。方法: 实验应用骨肉瘤细胞MG63作为研究对象,分5组。空白组、甘草次数组(50 μmol/L、100 μmol/L和200 μmol/L)、阳性对照组。每组6个复孔。空白组为不含有甘草次酸的DMEM的培养基,甘草次酸组分别加入50 μmol/L、100 μmol/L和200 μmol/L的甘草次酸,阳性对照组加入白藜芦醇(40 μmol/L)。将细胞接种于培养瓶内,当细胞进入生长平台期后使用0.1%的胰酶消化并按1×10⁶ cells/ml的密度接种于96孔板中,继续培养24 h。采用甲基四氮唑蓝检测细胞的增长率,Annexin V / PI双标记流式细胞术检测骨肉瘤细胞MG63的凋亡,蛋白质印迹法检测NF-κB蛋白的表达。结果: 与空白对照组相比,甘草次酸孵育24 h后,各组的骨肉瘤细胞G63增殖率明显降低 (P＜0.05)、凋亡细胞比例明显升高(P＜0.05);甘草次酸孵育48 h后,骨肉瘤细胞G63增殖率和NF-κB蛋白的相对表达量均明显降低(P＜0.05)、凋亡细胞比例明显升高(P＜0.05)。与阳性对照组比较,甘草次酸孵育24 h后,50 μmol/L甘草次酸组的细胞增殖率显著增高、100 μmol/L和200 μmol/L甘草次酸组的骨肉瘤细胞的增殖率显著降低(P＜0.05),甘草次酸孵育48 h后,50 μmol/L组和100 μmol/L组骨肉瘤细胞的增殖率显著升高,而200 μmol/组显著降低(P＜0.05);甘草次酸孵育24 h后,50 μmol/L、100 μmol/L和200 μmol/L组的骨肉瘤细胞的凋亡率均显著降低 (P＜0.05);而甘草次酸孵育48 h后,50 μmol/L、100 μmol/L组的骨肉瘤细胞的凋亡率也显著降低,而200 μmol/L组的凋亡率则显著升高。各剂量组间比较,200 μmol/L甘草次酸组的效果最佳,差异有显著性(P＜0.05);孵育48 h后,200 μmol/L甘草次酸组的效果无论在骨肉瘤细胞的增殖率还是凋亡比例其效果均优于阳性对照组(P＜0.05)。结论: 甘草次酸对骨肉瘤细胞G63增殖有抑制作用,其机制可能通过影响NF-κB信号通路,达到抑制骨肉瘤细胞MG63 增殖的作用。     

胞浆型磷脂酶A2介导弱氧化修饰低密度脂蛋白诱导的人脐静脉内皮细胞凋亡

探讨弱氧化修饰低密度脂蛋白(MM-LDL)能否诱导人脐静脉内皮细胞(HUVECs)凋亡以及胞浆型磷脂酶A2(cPLA2)在此过程中的作用.MTT法测定细胞存活率;相差显微镜、荧光显微镜和流式细胞仪检测细胞凋亡;3H-花生四烯酸(3H-AA)预标法测定PLA2活性;蛋白质印迹检测cPLA2磷酸化;激光共聚焦显微镜检测单个细胞内钙离子浓度的变化.结果表明,MM-LDL(100～300 mg/L)作用后的HUVECs呈现凋亡典型的形态特征,凋亡率随MM-LDL浓度的增加而上升.MM-LDL能引起胞内钙离子浓度增加,cPLA2的活化及磷酸化.15 μmol/L AACOCF3和5 mmol/L EGTA在抑制cPLA2活性的同时,部分抑制MM-LDL诱导的HUVECs凋亡.加入外源性AA(50 μmol/L)能逆转AACOCF3引起的凋亡抑制.结果提示,cPLA2参与了MM-LDL诱导HUVECs凋亡的信号传递.     

棉酚对Jurkat T细胞增殖与凋亡的影响

研究棉酚(gossypol)对Jurkat T细胞增殖和凋亡的影响及可能机制.将不同浓度的棉酚作用于Jurkat T细胞,用MTS比色法检测细胞存活率;以膜联蛋白V-PE染色分析细胞凋亡;用Hoechst33342染色观察核形态:用荧光染料Mitocapture结合流式细胞术和激光共焦显微镜检测线粒体跨膜电位变化.结果显示棉酚作用Jurkat T细胞24 h、48 h、72 h,其IC50值分别为77.2μmol/L、57.3 μmol/L、23.3 μmol/L,对细胞的抑制作用与药物存在时间-剂量依赖关系;终浓度为8、16、32 μmol/L的棉酚处理24 h后的细胞凋亡率分别为5.30%、15.20%、51.19%,对照组凋亡率为3.43%;高浓度棉酚作用后大量细胞核呈现染色质固缩、核碎裂和致密浓染等凋亡特征;随着浓度增加细胞线粒体跨膜电位明显降低.研究表明棉酚能有效抑制Jurkat T细胞增殖和诱导其发生凋亡,并呈现出时间-剂量依赖关系,其诱导凋亡的作用可能依赖于线粒体途径.     

垂体腺苷环化酶激活多肽抑制β淀粉样蛋白对Neuro-2a细胞神经毒性作用的机制

通过MTT方法检测细胞活性 ,同时采用激光共聚焦显微镜技术检测细胞内游离钙离子的瞬时运动 ,研究了垂体腺苷环化酶激活多肽 (pituitaryadenylatecyclaseactivatingpolypeptide 2 7,PACAP2 7)通过调节细胞内钙对抗淀粉样蛋白Aβ2 5 35引起Neuro 2a细胞神经毒性作用的可能机制。结果表明 ,PACAP在一定浓度范围内 (<0 1μmol/L)可提高Neuro 2a细胞增殖能力并对抗Aβ引起的神经毒性 ,此作用可以被PACAP受体竞争性拮抗剂PACAP6 2 7所抑制。 2 5 μmol/LAβ使细胞内钙离子缓慢上升 ,并有一个较长时间的平台期。 0 1μmol/L的PACAP使细胞内钙离子迅速升高后下降 ,10min后回到接近基线水平 ,伴有较长时间的不应期。用PACAP预处理细胞 10min后Aβ引起细胞内钙的慢上升不再出现。推测 ,PACAP受体激活引起瞬时内向钙离子运动 ,而后伴随一个较长时间的不应期 ,可能是一个消除凋亡或阻止凋亡启动的保护机制。     

甘草次酸对甲状腺癌细胞SW579 凋亡的影响及其机制*

目的:研究甘草次酸对甲状腺癌细胞SW579凋亡的影响及其可能的机制。方法:甲状腺癌细胞SW579分成4组,每组设置5个复孔,对照组为含10%胎牛血清的DMEM培养基;低浓度甘草次酸组为含浓度50 μmol/L+ 10%胎牛血清的DMEM培养基;中浓度甘草次酸组为含浓度100 μmol/L+ 10%胎牛血清的DMEM培养基;高浓度甘草次酸组为含浓度200 μmol/L+ 10%胎牛血清的DMEM培养基;各组在5%的二氧化碳培养箱中孵育24 h和48 h后,通过Annexin V / PI双标记流式细胞术检测甲状腺癌细胞SW579的凋亡比例,蛋白质印迹法检测检PI3K、AKT1、p-AKT蛋白的表达。结果:与对照组比较,孵育24 h及48 h后,50 μmol/L甘草次酸组凋亡细胞比例有所升高,AKT1、p-AKT、PI3K蛋白的相对表达量变化不明显,均无显著性差异(P＞0.05);100 μmol/L和200 μmol/L甘草次酸组的凋亡细胞比例均显著升高,AKT1、p-AKT蛋白的相对表达量均明显降低 (P＜0.05)。结论:100 μmol/L和200 μmol/L的甘草次酸可通过抑制AKT蛋白的表达促进甲状腺癌细胞SW579 凋亡。     

靶向探针追踪Aβ_(25-35)的亚细胞定位并基于Nrf2通路探讨阿里红多糖对线粒体损伤的保护机制

用靶向探针追踪淀粉样蛋白(Aβ_(25-35))的亚细胞定位情况,同时基于Nrf2信号通路探讨阿里红多糖组分(FOAPs-a)和(FOAPs-b)对Aβ_(25-35)诱导的PC12细胞线粒体损伤通路的保护作用机制。采用40μmol/L Aβ_(25-35)诱导PC12细胞建立阿尔茨海默病(AD)细胞模型,将PC12细胞分为空白组、模型组(加40μmol/L Aβ_(25-35))、阳性组(加50μmol/L盐酸多奈哌齐)、不同浓度的FOAPs-a和FOAPs-b干预组(各50、100、200μg/mL)。以靶向探针追踪Aβ_(25-35)在各组PC12细胞中的亚细胞定位情况;通过试剂盒检测PC12细胞中活性氧自由基ROS的变化情况;Western blotting法测定细胞凋亡相关蛋白Bax及Bcl-2的表达量以及和Nrf2通路相关的Nrf2、APK1和磷酸化的APK1蛋白的表达情况。结果发现,Aβ_(25-35)处理PC12细胞会影响线粒体的完整性;在200μg/mL FOAPs-a/b预处理PC12细胞后,能够显著缓解Aβ_(25-35)对线粒体的损伤,同时使Aβ_(25-35)的亚细胞共定位减弱;与空白组比较,模型组细胞中ROS含量增加,与模型组比较,FOAPs-a及FOAPs-b干预组均能降低ROS的沉积,差异有统计学意义;Western blotting结果显示:与模型组比较FOAPs-a及FOAPs-b均能减少APK1的磷酸化水平,上调Nrf2的蛋白表达水平。总之Aβ_(25-35)可进入到PC12细胞的线粒体中引起其损伤,阿里红多糖组分能够通过激活Nrf2信号通路显著缓解Aβ_(25-35)对PC12细胞线粒体的损伤。     

Ap5A延迟TRAIL诱导Novikoff细胞的凋亡

通过荧光分子标记和CONFOCAL技术检测方法,建立了TRAIL（TNF-related apoptosis inducing ligand, 一种类肿瘤坏死因子）诱导Novikoff细胞凋亡的模型,并探讨了TRAIL诱导凋亡的机制和Ap5A（P¹, P⁵-Di（adenosine-5′）pentaphosphate）在其中的作用.结果显示：TRAIL可诱导Novikoff细胞凋亡,且具有剂量和时间依赖性,同时胞内钙离子浓度显著上调.Ap5A能延迟TRAIL诱导的Novikoff细胞凋亡,同时下调胞内钙离子浓度.TRAIL和Ap5A分别上调和下调胞内钙离子浓度的作用可能是其诱发和延迟Novikoff细胞凋亡的一个机制.     

β-淀粉样蛋白通过激活caspase-3诱导PC12细胞凋亡

目的探讨β-淀粉样蛋白25-35片段（Aβ25-35）对体外培养的大鼠嗜铬瘤细胞PC12细胞促凋亡机制。方法采用四甲基偶氮唑蓝（MTT）法观察不同浓度的Aβ25-35干预PC12细胞24h后的细胞活性;将细胞分为对照组、实验组（即20 mmol/L Aβ25-35组）,流式细胞技术观察两组PC12细胞凋亡率;免疫细胞化学染色法观察PC12细胞凋亡基因caspase-3的表达。结果PC12细胞活性呈Aβ25-35剂量依赖性降低,且浓度为20 mmol/L时降低最显著;PC12细胞实验组的凋亡率为23.03%±1.22%,对照组为2.42%±0.87%（P〈0.01）;caspase-3实验组的阳性表达较对照组明显增加（P〈0.01）。结论Aβ可通过激活促凋亡基因caspase-3诱导PC12细胞凋亡。     

糖皮质激素快速抑制高钾离子诱导嗜铬细胞瘤细胞内游离钙浓度升高的作用及其特征

本研究应用钙离子特异荧光指示剂Fura-2/AM,使用Miracal影像系统(Miracal Image System)检测了糖皮质激素对高钾离子升高嗜铬细胞瘤细胞(PC12细胞)内游离钙浓度([Ca2+]i)作用的影响.结果表明:(1)皮质酮抑制高钾离子诱导PC12细胞[Ca2+]i升高与其预处理细胞时间的长短有关,预处理3 min时,皮质酮开始产生抑制作用;预处理5 min时,其呈现的抑制作用最强;预处理25 min时,抑制作用基本消失.(2)皮质酮在10-8～10-5 mol/L范围内时可呈剂量-效应关系,抑制高钾离子诱导的PC12细胞[Ca2+]i升高,皮质酮浓度为10-5 mol/L时,其产生的抑制作用最大;在10-9mol/L时抑制作用不明显.(3)其它甾体激素如皮质醇、地塞米松、孕酮、雌二醇、睾酮、醛固酮在浓度为10-5 mol/L时,也能抑制高钾离子引起的PC12细胞[Ca2+]i升高,但在同一浓度时作用强度有所不同.胆固醇浓度为10-5 mol/L时,对高钾离子诱导PC12细胞钙浓度升高没有抑制作用.在同一浓度时它们的作用强度顺序大致为:孕酮=皮质醇＞地塞米松＞睾酮＞醛固酮=雌二醇＞＞胆固醇.(4)在皮质酮浓度为10-5mol/L时不能抑制由细胞外无钙到有钙过程引起的PC12细胞[Ca2+]i升高.     

Puerarin protects PC12 cells against beta-amyloid-induced cell injury

beta-Amyloid protein (Abeta), a major protein component of brain senile plaques in Alzheimer's disease, is known to be directly responsible for the production of reactive oxygen species (ROS) and induction of apoptosis. In this study, the protective effect of puerarin, an isoflavone purified from the radix of the Chinese herb Pueraria lobata, on Abeta-induced rat pheochromocytoma (PC12) cultures was investigated. Although exposure of PC12 cells to 50 microM Abeta25-35 caused significant viability loss and apoptotic rate increase, pretreatment of the cells with puerarin for 24h reduced the viability loss and apoptotic rate. Puerarin (1 microM) significantly inhibited Abeta25-35-induced apoptosis of PC12 cells. Preincubation of the cell with puerarin also restored the ROS and mitochondrial membrane potential levels that had been altered as a result of Abeta25-35 treatment. Puerarin was also found to increase the Bcl-2/Bax ratio and reduce caspase-3 activation. These results suggest that puerarin could attenuate Abeta25-35-induced PC12 cell injure and apoptosis and could also promote the survival of PC12 cells. Therefore, puerarin may act as an intracellular ROS scavenger, and its antioxidant properties may protect against Abeta25-35-induced cell injury.     

锌离子调节皮质酮对原代培养大鼠海马神经元的损伤

探讨皮质酮对原代培养大鼠海马神经元的损伤效应及锌的调节作用。用原位染色和RT-PCR方法,分别检测神经元的损伤情况及NMDA受体三种亚基(NRl、NR2A、NR2B)mRNA的表达。皮质酮(5μmol／L)作用2,4h可明显降低海马神经元的存活率,导致神经元凋亡,并随着作用时间的延长而加重;锌离子明显影响皮质酮对海马神经元的损伤效应：同时加入皮质酮和低、中浓度Zn^2 (10、100μmol／L),可明显降低神经元凋亡率,而加入高浓度Zn^2 (250μmol／L)则加重神经元损伤。皮质酮作用24h后,海马神经元NRl、NR2BmRNA的表达水平增高,而同时加入低、中浓度Zn^2 (10、100μmol／L)的海马神经元NRl、NR2BmRNA表达水平与对照组接近;NR2AmRNA表达无明显变化。这些结果表明,锌对皮质酮所致应激损伤的调节具有双向性;NMDA受体亚基水平的变化可能是其中重要环节之一。     

Beta-amyloid increases somatostatin expression in cultured cortical neurons

In beta-amyloid (Abeta)-induced neurotoxicity, activation of the NMDA receptor, increased Ca2+ and oxidative stress are intimately associated with neuronal cell death as normally seen in NMDA-induced neurotoxicity. We have recently shown selective sparing of somatostatin (SST)-positive neurons and increased SST expression in NMDA agonist-induced neurotoxicity. Accordingly, the present study was undertaken to determine the effect of Abeta25-35-induced neurotoxicity on the expression of SST in cultured cortical neurons. Cultured cortical cells were exposed to Abeta25-35 and processed to determine the cellular content and release of SST into medium by radioimmunoassay and SST mRNA by RT-PCR. Abeta25-35 induces neuronal cell death in a concentration- and time-dependent fashion, increases SST mRNA synthesis and induces an augmentation in the cellular content of SST. No significant changes were seen on SST release at any concentration of Abeta25-35 after 24 h of treatment. However, Abeta25-35 induces a significant increase of SST release into medium only after 12 h in comparison with other time points. Most significantly, SST-positive neurons are selectively spared in the presence of a lower concentration of Abeta25-35, whereas, in the presence of higher concentrations of Abeta25-35 for extended time periods, SST-positive neurons decrease gradually. Furthermore, Abeta25-35 induces apoptosis at lower concentrations (5 and 10 micromol/L) and necrosis at higher concentrations (20 and 40 micromol/L). Consistent with the increased accumulation of SST, these data suggest that Abeta25-35 impairs cell membrane permeability. Selective sparing of SST-positive neurons at lower concentrations of Abeta25-35 at early time points directly correlates with the pathophysiology of Alzheimer's disease.     

一氧化氮对家兔房室结细胞自发活动的电生理效应

应用经典玻璃微电极技术,观察一氧化氮(NO)对家兔房室结细胞自发活动的电生理效应及其作用机制。结果显示：(1)NO供体硝普(SNP,1-1000μmol／L)及SIN-1(100,1000μmol／L)剂量依赖性地抑制房室结细胞的动作电位幅值(APA)、零相最大人士升速度(Vmax)、4期自动除极速度(VDD)及自发放电频率(RSF);(2)应用L型钙通道开放剂Bay K8644(0．25μmol／L),可拮抗SNP对房室结细胞的电生理效应;(3)提高灌流液中钙离子浓度(5mmol／L)也可逆转SNP对起搏细胞的抑制效应;(4)用无钙K-H液灌流房室结,可完全阻断SNP对房事结细胞的抑制效应。(5)应用鸟苷酸环化酶阻断剂甲基美蓝(50μmol／L)对SNP的上述电生理效应无影响。以上结果提示,NO可能是通过cGMP非依赖性途径减弱钙离子内流,进而抑制了家兔房室结细胞的自发电活动。     

菹草类胡萝卜素提取物对人肝癌细胞QGY-7703凋亡的影响

Human hepatoma cell line QGY-7703 was treated with the medium containing 10, 20, 40 and 60 micromol/L carotenoids extracts from Potamogoton crispus L. (CEPC) for 48 h, 96 h and 144 h, respectively. The inhibition rates to hepatoma cells were determined by MTT assay. The results showed the average inhibition rates of the three treatments varied from 0.14%-23.07%, 39.59%-70.61% and 71.65%-87.01%, respectively. After hepatoma cells were treated with the medium containing 10, 20 and 40 micromol/L of CEPC for 24 h, 48 h and 72 h, respectively, many typical morphology features of apoptotic cells were observed by Laser Scanning Confocal Microscope (LSCM), such as the distinct decrease in number and volume of cells, the shrinkage and deformation of cells, the shape of cell nucleuses appearing like crescent even piece, the decrease in area of yellow DNA in cell nuclei. The percentage of hepatoma cells in every phase of cell cycle was analyzed by Flow Cytometer (FCM) after being treated with 10 micromol/L and 20 micromol/L CEPC for 48 h. Compared with the control group, the cells in G0/G1 phase increased 23.8% (P<0.01) and 35.6% (P<0.01) respectively, in S phase decreased relevantly, while the cells in G2/M phase had no significant change. The Ca2+ concentration (fluorescence intensity) in cytoplasm of hepatoma cells was determined by LSCM after being treated with 20 micromol/L CEPC for 48 h. The Ca2+ concentration increased significantly (P<0.01) and was 1.5 times that of control group. These results demonstrated that the CEPC inhibited the proliferation of hepatoma cells QGY-7703 significantly in a dose and time-dependent manner in vitro. The hepatoma cells treated with CEPC were evidently arrested at G0/G1 phase in the cell cycle. The concentration of Ca2+ in test group cells cytoplasm increased significantly, it might be the important cause that CEPC induced the apoptosis of hepatoma cells QGY-7703. This paper provided scientific basis for further studying and developing the function and value of carotenoids in Potamogoton crispus L.     

Reconstitution of the basal calcium transport in resealed human red blood cell ghosts

The (45)Ca(2+) influx into right-side-out resealed ghosts (RG) prepared from human red blood cells (RBC) was measured. The (45)Ca(2+) equilibration occurred with t(1/2)=2.5 min and the steady-state was reached after 17 min with the level of 22+/-2 micromol/L(packed cells) at 37 degrees C. The rate of the influx was 97+/-17 micromol/L(packed cells)h. The (45)Ca(2+) influx was saturated with [Ca(2+)](0) at 4 mmol/L and was optimal at pH 6.5 and 30 degrees C. Divalent cations (10(-4)-10(-6)mol/L), nifedipine (10(-5)-10(-4)mol/L), DIDS (up to 10(-4)mol/L), and quinidine (10(-4)-10(-3)mol/L), inhibited the (45)Ca(2+) influx while uncoupler (10(-6)-10(-5)mol/L) stimulated it. In contrast to intact RBC, vanadate inhibited the (45)Ca(2+) influx when added to the external medium, however, the stimulation was observed when vanadate was present in media during both lysis and resealing. PMA had no effect under conditions found to stimulate the Ca(2+) influx in intact RBC. The results show that the Ca(2+) influx into RG is a carrier-mediated process but without control by protein kinase C and that the influx and efflux of Ca(2+) are coupled via the H(+) homeostasis similarly as in intact RBC but with modified mechanism.     

A specific inhibitor of cholesterol biosynthesis, BM15.766, reduces the expression of beta-secretase and the production of amyloid-beta in vitro

We have previously shown that statins reduce the production of amyloid-beta (Abeta) by both isoprenoid- and cholesterol-dependent mechanisms. These pathways contribute to the regulation of the dimerisation of BACE into its physiologically active form. Statins reduce cellular cholesterol levels by 20-40%; therefore, it is possible that the remaining cholesterol within the cell may play a significant role in the production of Abeta. Incubation of cells with the specific cholesterol biosynthesis inhibitor BM15.766 together with 50 micromol/L simvastatin and 400 micromol/L mevalonate reduced cellular cholesterol levels in a dose-dependent manner with increasing BM15.766 concentration (r = -0.9736, p = 0.0264). Furthermore, decreases in cellular cholesterol levels correlated with reductions in total Abeta production (r = 0.9683, p = 0.0317). A total of 2.5 micromol/L BM15.766 inhibited the dimerisation of BACE, whilst the expression of BACE monomer was reduced by 5 micromol/L BM15.766. BM15.766 treatment localised BACE predominantly within the Golgi, and reduced total BACE expression per cell. Similar changes were observed in the expression of the Golgi marker golgin-97, suggesting that reduced BACE expression may arise from a decrease in protein trafficking and an increase in degradation. By targeting cholesterol synthesis using specific cholesterol biosynthesis inhibitors, it is possible to reduce Abeta production without reducing protein isoprenylation.     

多巴胺对PC12细胞的双重影响

本实验运用PC12细胞,研究不同浓度多巴胺（dopamine,DA)对细胞的影响,同时利用兼具促进多巴胺释放和抑制多巴胺摄取双重作用的安排它命（amphetamine,AMP)观察胞内外多巴胺对细胞的不同作用。结果显示;胞外高浓度DA能引起细胞抗氧化能力下降,胞内游离Ca^2 浓度上升。细胞存活率大幅度降低,部分细胞出现凋亡;低浓度DA对细胞存活率无明显影响,而使细胞抗氧化能力有一定提高,长时间安非它命单独作用也可引起细胞存活率下降,并伴随胞内GSH水平降低;安非它命与多巴胺共同作用在一定程度上可导致细胞内抗氧化物质水平低于多巴胺单独作用,表明细胞内一定浓度DA可以维持或提高细胞抗氧化物质水平。结果提示,脑内同样存在的多巴胺神经元对DA重摄取功能下降,胞外氧化应激增强,可能是引起脑内多巴胺神经元退行性病变的重要原因之一。