Fang J, Zuo D M, Yu P H
Department of Psychiatry University of Saskatchewan, Saskatoon, Canada.
Life Sci. 1995;57(1):15-22. doi: 10.1016/0024-3205(95)00238-2.
R(-)-Deprenyl, an archetypical MAO-B inhibitor, has been shown to delay the onset of the disabling syndrome of Parkinson's disease and to be useful in the treatment of Alzheimer's disease. Recently, R(-)-deprenyl has been claimed to be capable of preventing apoptosis of PC12 cells, which had been primed with nerve growth factor (NGF) and followed by withdrawal of serum. We investigated the effect of R(-)-deprenyl in a non-neuronal cell model, namely, apoptosis of mouse thymocytes induced by dexamethasone. Trypan blue exclusion and lactate dehydrogenase activity were applied to assess the cell survival. R(-)-Deprenyl did not exhibit any detectable protective effect to the thymocytes from apoptosis. The result is further confirmed by examining the apoptotic DNA fragmentation using gel electrophoresis and assessing the soluble DNA released by a spectrophotometric method.
R(-)-司来吉兰，一种典型的单胺氧化酶-B抑制剂，已被证明可延缓帕金森病致残综合征的发作，并对阿尔茨海默病的治疗有效。最近，有人声称R(-)-司来吉兰能够预防经神经生长因子（NGF）预处理并随后血清撤除的PC12细胞的凋亡。我们在一个非神经元细胞模型中研究了R(-)-司来吉兰的作用，即地塞米松诱导的小鼠胸腺细胞凋亡。采用台盼蓝排斥法和乳酸脱氢酶活性测定来评估细胞存活情况。R(-)-司来吉兰对胸腺细胞凋亡未表现出任何可检测到的保护作用。通过凝胶电泳检测凋亡DNA片段化以及用分光光度法评估可溶性DNA释放，进一步证实了该结果。
