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首页> 外文期刊>Neuropathology: official journal of the Japanese Society of Neuropathology >Granzyme-b mediated cell death in the spinal cord-injured rat model.
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Granzyme-b mediated cell death in the spinal cord-injured rat model.

机译：脊髓损伤大鼠模型中粒酶b介导的细胞死亡。

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摘要

Spinal cord injury initiates a complex series of inflammatory and immune responses including the influx of monocytes, macrophages, T-cells, NK cells and so on, into the injured area. In the present study, we found a significant increase in the levels of granzyme-b (gra-b) from the first day after the transection until the third day, with decrease in intensity thereafter. The chemokine IP-10/CXCL10 was also found to be elevated along with gra-b correlating with the infiltration of CD-8(+) cytotoxic T lymphocytes (CTLs) into the injured spinal cord. We observed an increase in the levels of the 64 kDa poly ADP ribose polymerase fragment, known to be a signature fragment produced by gra-b. Localization of gra-b in TUNEL positive neurons indicates that gra-b might play a crucial role in neuronal death and contributes to the pathophysiology of spinal cord injury.
机译：脊髓损伤引发一系列复杂的炎症和免疫反应，包括单核细胞，巨噬细胞，T细胞，NK细胞等流入损伤区域。在本研究中，我们发现从横切后的第一天到第三天，颗粒酶b（gra-b）的水平显着增加，此后强度降低。还发现趋化因子IP-10 / CXCL10升高，并且与grab-b升高相关，后者与CD-8（+）细胞毒性T淋巴细胞（CTL）渗透到受伤的脊髓中有关。我们观察到64 kDa聚ADP核糖聚合酶片段（已知是gra-b产生的标记片段）水平增加。 gra-b在TUNEL阳性神经元中的定位表明gra-b可能在神经元死亡中起关键作用，并有助于脊髓损伤的病理生理。

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