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神经细胞

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Brain injury ; c-fos ; apoptosis ; neuroglial cell

脑损伤;基因;细胞凋亡;神经细胞

BMSCs can be induced into neural stem cells and further neural stem cells derived from bone marrow can differentiate into neural cells and neuroglial cells.

骨髓基质细胞能在体外诱导分化出神经干细胞,且骨髓源性神经干细胞可进一步定向分化为神经细胞及神经胶质细胞。

But in 24h experiment group, the decreases of the indexes are not statistically significant. Conclusion Early application of rhEPO could lessen the lesion of neuromotor function and secondary pathology change. The protection is partially due to the reduction of expression of Caspase-3 and neural cell apoptosis.

结果:与对照组相比,脊髓损伤后rhEPO1小时,6小时处理组神经运动功能和继发性病理损害明显改善,脊髓Caspase-3的表达明显下降(P 0.01);而术后24小时组与对照组相比,脊髓神经细胞凋亡指数及Caspase-3的表达下降均无统计学意义。

Activation of Fasl and Caspase3 may be related to cells apoptosis in the injured spinal cord. Early application of rhEPO could improve the neuromotor function. The protection is partially due to the reduction of neural cell apoptosis.

结论]早期应用外源性EPO对脊髓不完全损伤具有保护作用,可明显改善神经运动功能恢复情况,此种保护作用可能与EPO能够阻断Caspase3、fasfasl死亡蛋白途径的神经细胞凋亡有关。

It is different that different dose of NO influenced on incidence rate of neuronal apoptosis.

不同剂量的NO对神经细胞凋亡的影响不同。

It is defined as the strategy in treating a disease by preventing neuronal death.

神经保护是指以预防神经细胞死亡为目标的一种治疗方式。

Figure 4 it is a neuropathic changes with accumulated "ark neurone".

图4神经细胞散乱会引发一系列神经性疾病。

Olomoucine treatment can weaken the immunopathological damage and protect neurone, then improve the prognosis of HSE mice.

结论Olo-moucine治疗可以减弱HSE小鼠脑组织的免疫病理损伤,保护神经细胞,改善其预后。

FDP intervention decreases morphologic changes of mitochondria after HIBD, and may improve neuronic energy metabolism.

FDP干预治疗减轻了HIBD后脑神经细胞线粒体的形态变化并可能改善脑神经细胞的能量代谢。

Results Triglyceride droplets and giant mitochondrias were observed in hepatic cells, mitochondrias were damaged and lipofuscin increase in neuronic cells,observed apoptosis in both cells.

结果肝细胞内出现大量脂肪滴和巨大线粒体;神经细胞线粒体受损、脂褐质增多;发现凋亡细胞。

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