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6-甲酰四氢生物蝶呤对大鼠视网膜神经元短暂性缺血再灌注损伤的保护作用:一项形态学和免疫组织化学研究。

6-Formylpterin protects retinal neurons from transient ischemia-reperfusion injury in rats: a morphological and immunohistochemical study.

作者信息

Funakoshi Taisaku, Miyata Hajime, Imoto Toshiaki, Arai Toshiyuki, Endo Nobuyuki, Makino Keisuke, Yang Chun Hui, Ohama Eisaku

机构信息

Divisione of Ophthalmology and Visual Science, Department of Medicine of Sensory and Motor Organs, Faculty of Medicine, Tottori University, Yonago, Japan.

出版信息

Neuropathology. 2003 Sep;23(3):161-8. doi: 10.1046/j.1440-1789.2003.00493.x.

DOI:10.1046/j.1440-1789.2003.00493.x
PMID:14570282
Abstract

Neuroprotective effects of 6-formylpterin (6FP) on transient retinal ischemia-reperfusion injury were evaluated in rats by means of counting the number of retinal ganglion cells, measuring the thicknesses of the inner plexiform and inner nuclear layers, and by immunohistochemical detection of apoptotic cells in the retina. Sixty-one Sprague-Dawley rats (12 weeks, male, 295-330 g) were subjected to transient retinal ischemia-reperfusion by elevated intra-ocular pressure (80 mmHg for 60 min). Intraperitoneal injection of 6FP (3.8 mg/kg) was performed before or after ischemia. The retina was histologically better preserved in rats with 6FP treatment than without 6FP treatment. 6FP showed more strong neuroprotective effects when it was administered before ischemia. The number of single-stranded DNA-positive cells in the retina also decreased remarkably in rats with 6FP treatment, especially when administered before ischemia. These results suggest that 6FP protects retinal neurons from transient ischemia-reperfusion injury, at least in part by inhibiting apoptotic cell death.

摘要

通过计数视网膜神经节细胞数量、测量内网状层和内核层厚度以及免疫组织化学检测视网膜中的凋亡细胞,评估了6-甲酰蝶呤(6FP)对大鼠短暂性视网膜缺血再灌注损伤的神经保护作用。61只Sprague-Dawley大鼠(12周龄,雄性,体重295 - 330克)通过升高眼压(80 mmHg,持续60分钟)进行短暂性视网膜缺血再灌注。在缺血前或缺血后腹腔注射6FP(3.8毫克/千克)。组织学检查显示,接受6FP治疗的大鼠视网膜比未接受6FP治疗的大鼠保存得更好。当在缺血前给予6FP时,其显示出更强的神经保护作用。接受6FP治疗的大鼠视网膜中单链DNA阳性细胞数量也显著减少,尤其是在缺血前给予6FP时。这些结果表明,6FP可保护视网膜神经元免受短暂性缺血再灌注损伤,至少部分是通过抑制凋亡细胞死亡来实现的。

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