Study on Molecular Mechanism and Therapy of Light-induce Retinal Damage
光致视网膜损伤的分子机制及治疗研究
基本信息
- 批准号:14571673
- 负责人:
- 金额:$ 2.18万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2002
- 资助国家:日本
- 起止时间:2002 至 2003
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
PURPOSE. To examine our hypothesis that glutathione peroxidase (GPX) is induced at different time points after retinal light exposure and localizes in different retinal cells.METHODS. The rats were kept cyclic light for 2 weeks before the experiments. The animals were maintained in 12-hour cycles of light and dark before and after exposure to intense white fluorescent light for as long as 24 hours and then returned to cyclic light. GPX expression was measured by immunohisto-cytochemistry, Western, and Northern blots. Light-induced retinal damage was determined by the outer nuclear layer (ONL) thickness relative to the total retinal thickness.RESULTS. GPX labeling was not seen in the photoreceptor inner segments and slight labeling was observed in the photoreceptor outer segments or the retinal pigment epithelial (RPE) cells in the normal retina kept in cyclic light. In retinal specimens maintained in light for 12 and 24 hours GPX labeling was induced in the photoreceptor outer segments … More and RPE cells. High GPX expression in the retinal pigment, epithelium was sustained until day 7 after challenge. In contrast, GPX expression in the photoreceptor outer segments decreased on day 1 and disappeared on days 3 and 7 after exposure. Intense GPX labeling was seen from the internal limiting membrane to fan lion cell layer. GPX labeling was constantly localized in both high-intensity white light and cyclic conditions, suggesting no induction of GPX in those areas. In addition, GPX labeling was apparent at the posterior retinal pole but not at the peripheral retina. We observe marked upregulation of GPX mRNA in rats kept in high-intensity white light. One, 3 and 7 days after exposure to high-intensity white light, there was a significant difference (P<0.0001) between the control and experimental groups in the ratio of the outer nuclear layer thickness to the entire retina.CONCLUSIONS. GPX was Induced at different time points after exposure to high-intensity white light and localized in different retinal cells. Changes in GPX expression after light exposure may, be related to the difference in light-damage susceptibility of the retina. Less
目的。为了研究我们的假设,即在视网膜光暴露后在不同的时间点诱导了谷胱甘肽过氧化物酶(GPX),并将其定位于不同的视网膜细胞。在实验之前,将大鼠保持环状光度2周。在暴露于强烈的白色荧光灯之前和之后,将动物保持在12小时的光和黑暗周期中长达24小时,然后返回到环状光线。 GPX表达是通过免疫史 - 环化学,西部和北印迹测量的。光引起的视网膜损伤是通过外核层(ONL)厚度相对于总残留厚度确定的。在光感受器的内部段中未观察到GPX标记,并且在光感受器的外部段或视网膜色素上皮(RPE)细胞中观察到略微标记,在正常视网膜中保持在环状光中。在光线受体外部段中诱导了在光线下保持12和24小时的残留标本中,更多的gpx标记……更多和RPE细胞。在视网膜色素中,高度GPX表达,上皮一直持续到挑战后的第7天。相比之下,光感受器外部段中的GPX表达在第1天减少,在暴露后第3和第7天消失。从内部极限膜到扇形狮细胞层可以看到强烈的GPX标记。 GPX标记在高强度的白光和循环条件下都经常定位,表明这些区域没有GPX诱导。此外,GPX标记在后视网膜后明显是显而易见的,但在周围视网膜上不明显。我们观察到在保持高强度白光的大鼠中GPX mRNA的明显上调。暴露于高强度白光后的一,3和7天,对照组和实验组之间在外核层厚度与整个视网膜的比率之间存在显着差异(p <0.0001)。暴露于高强度白光后,在不同时间点诱导了GPX,并局部在不同的视网膜细胞中。暴露后GPX表达的变化可能与视网膜的轻伤敏感性差异有关。较少的
项目成果
期刊论文数量(8)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Akihiro Ohira, Masaki Tanito, Sachiko Kaidzu, Takahito Kondo: "Glutathione peroxidase induced in rat retinas to counteract photic injury,"Investigative Ophthalmology & Visual Science. 44(3). 1230-1236 (2003)
Akihiro Ohira、Masaki Tanito、Sachiko Kaidzu、Takahito Kondo:“在大鼠视网膜中诱导谷胱甘肽过氧化物酶以抵消光损伤”,调查眼科
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M.Tanito, T.Takanashi, S.Kaidzu, Y.Yoshida, A.Ohira: "Cytoprotective effects of rebamipide and carteolol hydrochloride against ultravioletB-induced corneal damage in mice"Investigative Ophthalmology and Visual Science. 44(7). 2980-2985 (2003)
M.Tanito、T.Takanashi、S.Kaidzu、Y.Yoshida、A.Ohira:“瑞巴派特和盐酸卡替洛尔对 UVB 诱导的小鼠角膜损伤的细胞保护作用”研究眼科和视觉科学。
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- 影响因子:0
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Ohira A, Tanito M, Kaidzu S, Kondo T.: "Glutathione peroxidase induced in rat retinas to counteract photic injury"Invest Ophthalmol Vis Sci. 44(3). 1230-1236 (2003)
Ohira A、Tanito M、Kaidzu S、Kondo T.:“在大鼠视网膜中诱导谷胱甘肽过氧化物酶以抵消光损伤”Invest Ophasemol Vis Sci。
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- 影响因子:0
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Masaki Tanito, Taiji Takanashi, Sachiko Kaidzu, Yasukazu Yoshida, Akihiro Ohira: "Cytoprotective effects of rebamipide and carteolol hydrochloride against ultraviolet B-induced corneal damage in mice"Ophthalmology & Visual Science. 44(7). 2980-2985 (2003)
Masaki Tanito、Taiji Takanashi、Sachiko Kaidzu、Yasukazu Yoshida、Akihiro Ohira:“瑞巴派特和盐酸卡替洛尔对紫外线 B 诱导的小鼠角膜损伤的细胞保护作用”
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- 发表时间:
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- 影响因子:0
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M.Tanito, T.Takanashi, S.Kaidzu, Y.Yoshida, A.Ohira: "Cytoprotective effects of rebamipide and carteolol hydrochloride against ultraviolet B-induced corneal damage in mice"Investigative Ophthalmology and Visual Science. 44(7). 2980-2985 (2003)
M.Tanito、T.Takanashi、S.Kaidzu、Y.Yoshida、A.Ohira:“瑞巴派特和盐酸卡替洛尔对紫外线 B 诱导的小鼠角膜损伤的细胞保护作用”研究眼科和视觉科学。
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OHIRA Akihiro其他文献
OHIRA Akihiro的其他文献
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{{ truncateString('OHIRA Akihiro', 18)}}的其他基金
Studies on how lutein administration enhances antioxidant capacity by increasing reduced thiols
叶黄素给药如何通过增加还原硫醇来增强抗氧化能力的研究
- 批准号:
18K09448 - 财政年份:2018
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Study of Pathological Mechanism in Light Induced Retinal Damage using DNA Base Excision Repair Gene Knockout Mice
DNA碱基切除修复基因敲除小鼠光致视网膜损伤病理机制研究
- 批准号:
23592570 - 财政年份:2011
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The development of new retinal oxidative stress market and the effects of vitamin E intensive care against retinal light damage
视网膜氧化应激新市场的发展及维生素E重症监护对抗视网膜光损伤的作用
- 批准号:
18591921 - 财政年份:2006
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Cytoprotection of prostaglandin under oxidative stress
氧化应激下前列腺素的细胞保护
- 批准号:
11671739 - 财政年份:1999
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Defense mechanism for age-related macular degeneration.
年龄相关性黄斑变性的防御机制。
- 批准号:
09671806 - 财政年份:1997
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Defense mechanism for retinal light damage.
视网膜光损伤的防御机制。
- 批准号:
06671769 - 财政年份:1994
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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