目的：观察美洛昔康对慢性铝过负荷致大鼠神经元退变的保护作用及其机制。
Objective To study the protective effects and mechanisms of meloxicam on neurodegeneration induced by chronic aluminum overload in rats.
侧脑室微量注射氯化铝，一天1次，连续5天，建立铝负荷致小鼠神经元退变模型。
Methods(1) Neurodegenerative model of mice was established via intracerebroventricular injection of aluminum, once a day for 5 days.
结果（1）基因工程细胞可防止多巴胺能神经元退变死亡，与对照组比较，最多增加了95 4 %，P。
Results The number of dopaminergic neurons protected by engineered cells increased at least by 95.4% in comparison with the control cells (P<0.01).
越来越多的研究结果提示，COX - 2和5 - LO及其催化产物可能与神经元损伤和神经元退变有关。
More and more studies suggest that COX-2 and 5-lox, as well as their products be involved in neuron damage and neurodegeneration.
在本研究中，我们试图对COX - 2和5 -LO的表达与铝过负荷致神经元退变的关系进行初步研究。方法。
In this study we try to elucidate the relationship between expression of 5-lox and COX-2 and neurodegeneration induced by aluminum overload.
尽管其对于中枢神经系统的作用目前并不十分清楚，大量研究表明，5lox参与了生理状态下的脑细胞增殖，并在神经元退变中扮演了重要角色。
Although its role in CNS is not completely clear, studies showed that 5lox appear to be associated with neuron proliferation in physiological status and may participate in CNS neurodegeneration.
本文探讨了脑源性神经营养因子、神经生长因子对体外长期培养的胚基底前脑胆碱能神经元是否具有延缓退变的作用。
The delaying effects of BDNF and NGF on the degeneration of the long term cultured embryonic basal forebrain cholinergic neurons in vitro were studied.
本文探讨了脑源性神经营养因子、神经生长因子对体外长期培养的胚基底前脑胆碱能神经元是否具有延缓退变的作用。
The delaying effects of BDNF and NGF on the degeneration of the long term cultured embryonic basal forebrain cholinergic neurons in vitro were studied.
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