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[白质损伤新生大鼠中诱导型一氧化氮合酶蛋白表达与神经胶质细胞凋亡]

[Expression of iNOS protein and gliacyte apoptosis in neonatal rats with white matter damage].

作者信息

Wang Hui-Qing, Xiong Ying, Guo Wen-Jun

机构信息

Department of Neonatology, West China Second University Hospital of Sichuan University, Chengdu 610041, China.

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2011 Apr;13(4):309-12.

PMID:21507301
Abstract

OBJECTIVE

Inducible nitric oxide synthase (iNOS) is a main rate-limiting enzyme resulting in over-production of nitric oxide following hypoxia-ischemia (HI). The aim of this study was to observe the expression of iNOS protein and gliacyte apoptosis in the brains of premature rats after HI, in order to explore possible relationships of iNOS with white matter damage (WMD).

METHODS

One hundred and twelve 2-day-old premature rats were randomly subjected to right carotid ligation followed by 4 hrs hypoxic stress (WMD group) or sham operation (control group). The pups were sacrificed at 1, 3, 6, 12 hrs, and 1, 3 and 7 days after HI. Immunohistochemical technique was applied to determine the iNOS expression in periventricular white matter tissues. Gliacyte apoptosis was detected in these tissues by TUNEL.

RESULTS

Compared with the control group, iNOS expression began to increase 1 hr after HI and reached the peak 1 day after HI in the WMD group. Gliacyte apoptosis increased 1 hr after HI and peaked 1 day after HI in the WMD group compared with the control group.

CONCLUSIONS

In the neonatal rats with WMD, the expression of iNOS may be involved in the ischemic cellular events including apoptosis, and plays a role in the pathophysiological process of WMD.

摘要

目的

诱导型一氧化氮合酶(iNOS)是缺氧缺血(HI)后导致一氧化氮过量产生的主要限速酶。本研究旨在观察HI后早产大鼠脑内iNOS蛋白表达及神经胶质细胞凋亡情况,以探讨iNOS与白质损伤(WMD)之间可能的关系。

方法

112只2日龄早产大鼠随机分为右侧颈动脉结扎并给予4小时缺氧应激组(WMD组)和假手术组(对照组)。在HI后1、3、6、12小时以及1、3和7天处死幼鼠。采用免疫组织化学技术检测脑室周围白质组织中iNOS的表达。通过TUNEL法检测这些组织中的神经胶质细胞凋亡情况。

结果

与对照组相比,WMD组中HI后1小时iNOS表达开始增加,HI后1天达到峰值。与对照组相比,WMD组中HI后1小时神经胶质细胞凋亡增加,HI后1天达到峰值。

结论

在患有WMD的新生大鼠中,iNOS的表达可能参与包括凋亡在内的缺血性细胞事件,并在WMD的病理生理过程中起作用。

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