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[缺血再灌注后小鼠视网膜中核因子κB的激活]

[Activation of NF-kappa B in the mouse retina after ischemia reperfusion].

作者信息

Chen Yue-guo, Zhang Cheng, Wu Ting-huai, Jiang Jian-sen, Tso Mark

机构信息

The Third Clinical School of Peking University, Peking University Eye Center, Beijing 100083, China.

出版信息

Zhonghua Yan Ke Za Zhi. 2003 Sep;39(9):560-4.

Abstract

OBJECTIVE

To investigate the expression of NF-kappa B following retinal ischemia and reperfusion injury in mice.

METHODS

Retinal ischemia was induced by elevation of intraocular pressure. Retinal degeneration and atrophy were quantified by an image analysis system. Immunohistochemistry using p65 monoclonal antibody was performed on the retina and co-related with TUNEL labeling.

RESULTS

Inner retinal thickness was increased in the initial 24 hours following retinal ischemia and was ascribed to tissue edema, but was significantly decreased by 168 hours after reperfusion. Six hours after retinal ischemia, p65 immunoreactivity was increased in the ganglion cell and the inner nuclear layers, reached a peak at 24 hours, and was parallel to TUNEL labeling. Double labeling with p65 and TUNEL showed partial co-localization of p65 and TUNEL labeling, predominantly in the inner nuclear layer.

CONCLUSIONS

Activation of NF-kappa B appears to play an important role in retinal degeneration following retinal ischemia and reperfusion injury. The pro- and anti-apoptotic effects of NF-kappa B after retinal ischemia are being further investigated.

摘要

目的

研究小鼠视网膜缺血再灌注损伤后核因子-κB(NF-κB)的表达情况。

方法

通过升高眼压诱导视网膜缺血。使用图像分析系统对视网膜变性和萎缩进行量化。用p65单克隆抗体对视网膜进行免疫组织化学检测,并与TUNEL标记相关联。

结果

视网膜缺血后的最初24小时内,视网膜内层厚度增加,这归因于组织水肿,但再灌注168小时后显著降低。视网膜缺血6小时后,神经节细胞层和内核层中p65免疫反应性增加,在24小时达到峰值,且与TUNEL标记平行。p65与TUNEL双重标记显示p65和TUNEL标记部分共定位,主要在内核层。

结论

NF-κB的激活似乎在视网膜缺血再灌注损伤后的视网膜变性中起重要作用。NF-κB在视网膜缺血后的促凋亡和抗凋亡作用正在进一步研究中。

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