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Cerebral ischemia preconditioning can protect the neuron against the injury of the fatal brain ischemia followed, reduce the quantity of dead parenchyma cell, deflate infarct volume, relieve neuralgic impairment, reduce the expression of IL-6, increase the expression of Ngb, reduce the neuronal degeneration, necrosis and tissue edema.

1。缺血预处理能对随后发生的再次脑缺血所致的神经元损伤起保护作用,减轻神经功能缺损症状,减小梗死体积,使海马区IL-6表达减少,皮质区Ngb表达上调,并减轻神经细胞变性、坏死。

The outer neuroblastic layer before it divided to inner and outer nuclear layer and outer complexiform layer and gonglion cell layer showed a temporal PCNA positive which was related to proliferation. The three cell layers had another PCNA positive when finished time changed from outer to inner after their morphologic development basically completed( outer nuclear layer:11~15 days,inner nuclear layer: 8~16 days, gonglion cell layer:16~21 days).

PCNA显示在外成神经细胞层分化为内、外核层和外丛状层之前,和节细胞各有一次和增殖相关的阳性表达。3个细胞层在形态学的分化基本完成后,又出现了一次结束时间是由外向内变化的阳性过程(外核层:第11天至15天:内核层:第8天至16天,神经节细胞层: 16天到21天,这一次阳性表达过程可见到细胞形态向成年形态的转化。

AIM: To study the protective effects of ceftriaxone on neurocyte and its mechanism.

目的:研究头孢曲松对神经细胞的保护作用及其机制。

Objective To study the effects of IL-1 receptor antagonist(IL-1ra)on neurocyte apoptosis in cerebral ischemia in rats.

目的 探讨白细胞介素1受体拮抗剂(IL-1ra)对大鼠局灶性脑缺血再灌注神经细胞凋亡的影响。

Objective: To study the expression of neurocyte apoptosis of thoracic spinal cord in rats with chronic fluorosis and discuss the related mechanism.

目的:探讨慢性氟中毒大鼠胸髓神经细胞的凋亡及其发生机制。

The co-cultured allogenic BMSCs can be induced into neurocyte such as neuron and glial cell in vitro.

同种异体共培养的骨髓间充质干细胞可在体外定向诱导为神经元和胶质细胞等神经细胞

Objective To study the pathology mechanism of vascular dementia rats and study the effect of Bushenxingnao prescription on cerebral neurocyte apoptosis.

目的 观察补肾醒脑方对血管性痴呆大鼠脑神经细胞凋亡的影响,探讨其病理机制。

Tongmai Yizhi decoction can reduce the damage of neurocyte by regulating the expression of nNOS.

通脉益智方通过调控nNOS的表达,减少神经细胞的损伤,增加学习和记忆功能。

Naloxone can play an role in the protection of brain through diminishing neurocyte apoptosis by promoting the expression of Bcl-2 and restraining the expression of Bax,p53 and Fas.

纳洛酮可能通过促进Bcl-2的表达和抑制Bax、p53、Fas的表达来减少脑复苏后神经细胞的凋亡而发挥其脑保护的作用。

Naloxone can play an role in the protection of brain through diminishing neurocyte apoptosis by promoting the expression of Bcl-2 and restraining the expression of Bax,p53 and Fas.

纳洛酮大概议决促进Bcl-2的表达和克制Bax、p53、Fas的表达来淘汰脑苏醒后神经细胞的凋亡而发挥其脑掩护的作用。

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