Kolla Nathan, Wei Zelan, Richardson J Steven, Li Xin-Min
Neuropsychiatry Research Unit, Department of Psychiatry, University of Saskatchewan.
J Psychiatry Neurosci. 2005 May;30(3):196-201.
To investigate the potential protective effects of amitriptyline and fluoxetine in a catecholamine cell model.
Cultured rat pheochromocytoma (PC12) cells were pretreated with amitriptyline or fluoxetine for 24 or 48 hours and were then subjected to neurotoxic insult (200 micromol/L hydrogen peroxide). Cell viability was determined by measurement of the reduction product of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). The enzyme activity of superoxide dismutase (SOD) was determined by a commercial SOD assay kit.
The decrease in cell viability induced by hydrogen peroxide was attenuated in PC12 cells pretreated with 100 micromol/L amitriptyline for 24 hours or with 50 micromol/L amitriptyline or 50 micromol/L fluoxetine for 48 hours. Pretreatment with either amitriptyline or fluoxetine was associated with increased SOD activity in PC12 cells. Inhibition of SOD activity with diethyldithiocarbamic acid reduced the cytoprotective action of fluoxetine.
These data suggest that the neuroprotective actions of some antidepressants include the upregulation of SOD activity.
研究阿米替林和氟西汀在儿茶酚胺细胞模型中的潜在保护作用。
将培养的大鼠嗜铬细胞瘤(PC12)细胞用阿米替林或氟西汀预处理24或48小时,然后进行神经毒性损伤(200微摩尔/升过氧化氢)。通过测量3-[4,5-二甲基噻唑-2-基]-2,5-二苯基四氮唑溴盐(MTT)的还原产物来测定细胞活力。用市售的超氧化物歧化酶(SOD)检测试剂盒测定SOD的酶活性。
在用100微摩尔/升阿米替林预处理24小时或用50微摩尔/升阿米替林或50微摩尔/升氟西汀预处理48小时的PC12细胞中,过氧化氢诱导的细胞活力下降得到缓解。用阿米替林或氟西汀预处理均与PC12细胞中SOD活性增加有关。用二乙基二硫代氨基甲酸盐抑制SOD活性可降低氟西汀的细胞保护作用。
这些数据表明,一些抗抑郁药的神经保护作用包括上调SOD活性。