Suppr超能文献

EGB761 对大鼠视网膜光损伤的作用。

EGB761 on retinal light injury in rats.

机构信息

Department of Ophthalmology, Shanghai Jiao Tong University Affiliated First People's Hospital, Shanghai 200080, China.

出版信息

Chin Med J (Engl). 2012 Jul;125(13):2306-9.

Abstract

BACKGROUND

Retinal light injury can lead to degeneration of the photoreceptor cell layer. It has been hypothesized that the mechanism for this process is the photochemical damage. Ginkgo balboa extract (Ginkgo biloba extract EGB761) EGB761 is a free radical scavenger. The purpose of this study was to investigate the possible effect of orally administered EGB761 on retinal light damage of mouse photoreceptor cells.

METHODS

Kunming mice were randomly chosen for the following groups containing 20 animals in each: control group, light damage group, saline control group, and drug treatment group. The drug treatment group and saline control group were given daily gavage of EGB761 (150 mg×kg(-1)×d(-1)) one week before light exposure. At 7, 14, and 30 days after light exposure, animals were sacrificed and eyes were examined by light microscopy, electron microscopy, and retinal histopathology using in situ detection of apoptotic cells.

RESULTS

In the light damage group after 7 days there was visible edema, and the outer nuclear layer appeared withered with deeply stained dead cells, leaving only a thin nuclear layer of 7 - 8 cells. After 14 days, the photoreceptor cell layer disappeared, leaving only the outer nuclear layer of 1 - 3 cells with an average thickness of (37.988 ± 1.207) µm. The average thickness of the retina was (126.32 ± 2.31) µm. In the drug treatment group, the photoreceptor cell layer and outer nuclear layer damage were significantly lower than the saline group (t = 21.993, P < 0.001), demonstrating that EGB761, especially at 14 days after light exposure, can reduce retinal light damage in mice.

CONCLUSION

Oral administration of EGB761 can partially inhibit apoptosis of photoreceptor cells, resulting in increased photoreceptor cell survival.

摘要

背景

视网膜光损伤可导致光感受器细胞层变性。据推测,该过程的机制是光化学损伤。银杏叶提取物(银杏叶提取物 EGB761)EGB761 是一种自由基清除剂。本研究旨在探讨口服给予 EGB761 对小鼠光感受器细胞视网膜光损伤的可能影响。

方法

昆明小鼠随机分为以下 4 组,每组 20 只:对照组、光损伤组、生理盐水对照组和药物治疗组。药物治疗组和生理盐水对照组在暴露于光前一周每天给予 EGB761(150mg×kg(-1)×d(-1))灌胃。在光暴露后 7、14 和 30 天处死动物,通过光镜、电镜和视网膜组织病理学检查,用原位检测凋亡细胞观察眼睛情况。

结果

在光损伤组,光暴露后 7 天可见明显水肿,外核层出现枯萎,深染死亡细胞,仅留下 7-8 层薄的核层。14 天后,光感受器细胞层消失,仅留下 1-3 层外核层,平均厚度为(37.988±1.207)µm。视网膜平均厚度为(126.32±2.31)µm。在药物治疗组,光感受器细胞层和外核层损伤明显低于生理盐水组(t=21.993,P<0.001),表明 EGB761,特别是在光暴露后 14 天,可以减轻小鼠视网膜光损伤。

结论

口服给予 EGB761 可部分抑制光感受器细胞凋亡,从而增加光感受器细胞的存活率。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验