Vitamin E renders protection to PC12 cells against oxidative damage and apoptosis induced by single-walled carbon nanotubes.
Vitamin E renders protection to PC12 cells against oxidative damage and apoptosis induced by single-walled carbon nanotubes.
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DOI：
10.1016/j.tiv.2011.10.004
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发表时间：
2012-02
期刊：
影响因子：
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通讯作者：
Jingyun Wang;Pingping Sun;Y. Bao;Bairui Dou;Dandan Song;Yachen Li
中科院分区：
文献类型：
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作者：
Jingyun Wang;Pingping Sun;Y. Bao;Bairui Dou;Dandan Song;Yachen Li
单壁碳纳米管（SWCNTs）在许多生物医学应用中是潜在的候选者。然而，许多报告显示其对人类和其他生物系统的潜在毒性。我们的研究表明，单壁碳纳米管可以诱导细胞凋亡和氧化损伤的PC 12细胞，在体外模型的神经细胞。在本研究中，我们首次研究了维生素E（VE）对SWCNT诱导的PC 12细胞神经毒性的神经保护作用。维生素E（0.01- 2 mM）以时间和剂量依赖的方式增加PC 12细胞的存活率并显著减弱SWCNT诱导的凋亡性细胞死亡，如3-（4，5-二甲基噻唑-2-基）-2，5-二苯基溴化四氮唑（MTT）测定、乳酸脱氢酶（LDH）释放和形态学观察所证明的。VE的存在抑制了活性氧（ROS）的形成，降低了脂质过氧化物的水平，提高了谷胱甘肽（GSH）的水平和超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）的活性。此外，VE阻断了线粒体膜电位的降低和caspase-3的激活。VE可抑制SWCNTs诱导的PC 12细胞Bcl-2表达下调和Bax表达上调。综上所述，VE可能通过下调氧化应激和抑制细胞凋亡来保护PC 12细胞免受SWCNTs的损伤。
Single-walled carbon nanotubes (SWCNTs) are potential candidates in many biomedical applications. However, many reports demonstrated its potential toxicity to human and other biological systems. Our study has demonstrated that SWCNTs can induce apoptosis and oxidative damage on PC12 cells, an in vitro model of neuronal cells. In the present study, we for the first time investigated the neuroprotective effects of vitamin E (VE) on SWCNT-induced neurotoxicity in cultured PC12 cells. Vitamin E (0.01–2mM) increased PC12 cells viability and significantly attenuated SWCNTs-induced apoptotic cell death in a time and dose-dependent manner, as demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, lactate dehydrogenase (LDH) release and morphological observation. The presence of VE inhibited the formation of reactive oxygen species (ROS), decreased the level of lipid peroxide, elevated the level of glutathione (GSH) and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Additionally, VE blocked the reduction in the mitochondrial membrane potential and the activation of caspase-3. VE prevented the down-regulation of Bcl-2 expression and up-regulation of Bax expression induced by SWCNTs in PC12 cells. In summary, VE might protect PC12 cells from the injury induced by SWCNTs through the down-regulation of oxidative stress and prevention of mitochondrial-mediated apoptosis.