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乙炔的选择性单胺氧化酶抑制剂(毛)B型自杀司立吉林(以前称为L-deprenyl)已被证明是一个有用的辅助左旋多巴治疗和单药治疗帕金森病(PD)。司立吉林很容易从胃肠道吸收,迅速进入大脑和脊髓后口服。药物结合高缺氧的大脑区域的内容,如丘脑、纹状体、皮质和脑干。人类广泛代谢,主要在肝脏形成desmethylselegiline和冰毒,进一步代谢安非他命。10毫克剂量的百分之八十六在尿液在24小时内恢复。这些数据表明,代谢产物积累不发生。虽然不是anti-PD行动是已知的所有特性,研究利用病人的大脑获得尸检处理10毫克的司立吉林表明选择性抑制缺氧,同时增加的苯乙胺和多巴胺(DA)但不是5 -羟色胺和去甲肾上腺素,在基底神经节可能被视为其作用方式。司立吉林在PD提供的保护作用,导致延迟左旋多巴治疗的需要,有着各种各样的解释方面的参与内源性神经毒素或氧自由基机制(氧化应激)在帕金森病的发展。然而,尽管有很多种不同的假设和最近的发现强调了意义的氧化应激在疾病的发病机制,导致慢性nigral细胞死亡和底层机制依然存在,到目前为止,难以捉摸。因此,没有明确的知识对于理解司立吉林的报道影响帕金森病的进展。 Nevertheless, selegiline might be expected to have some protective effects in reducing the production of potentially neurotoxic compounds resulting in the MAO-catalyzed oxidation of DA. In addition, some evidence suggests both an indirect (via induction of radical-scavenging enzymes) and a direct antioxidant function for selegiline. On the other hand, the reported protective effect of selegiline might also receive a contribution from the diminished potentiation of the N-methyl-D-aspartate receptor by the polyamine binding site. Finally, the effects of selegiline might also involve preventing, or perhaps to some extent reversing, the decline in resistance normally associated with cellular aging because of its neurotrophine-like action. However, even in the early clinical stage of PD, the sequence of events leading to nigral cell death may be too far advanced for selegiline to exhibit its maximum potential.
首页,85神经学1996;47 (24):S137-S145
- 版权1996年Advanstar通信公司。
