A research about the new therapy for glaucomatous optic nerve damage based on the endogenous neuroprotective system
基于内源性神经保护系统的青光眼视神经损伤新疗法研究
基本信息
- 批准号:14370561
- 负责人:
- 金额:$ 9.54万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 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
In this research, we investigated our hypothesis that immune reaction and stress response exerted neuroprotective effect on glaucomatous optic nerve damage. First, we reported that IL-6, multifunctional cytokine produced by several cells, provided a neuroproctive effect on retinal damage (BBRC 302:226,2003). Second, we demonstrated the neuroprotective effect of statin (Arch Ophthalmol 120:1707,2002) and antithrombin III (IOVS 44:332,2003) and the beneficial effects of anti-LOX-1 antibody on the endotoxin-induced inflammation (Pro Natl Acad Sci USA 100:1274,2003) by inhibiting leukocyte-endothelial interaction. Third, we demonstrated the neuroprotective effect of LEDGF, enodogenous and exogenous survival factor, on retinal damage (Brain Res 991:163,2003). Fourth, we elucidated the clinical and surgical outcomes of the treatment of unique type of secondary glaucoma associated with transthyretin related familial amyliod polyneuropathy (Arch Ophthalmol 121:351,2003).
本研究探讨了免疫反应和应激反应在青光眼视神经损伤中发挥神经保护作用的假说。首先,我们报道了IL-6,由几种细胞产生的多功能细胞因子,对视网膜损伤提供神经保护作用(BBRC 302:226,2003)。其次,我们证明了他汀类药物(Arch Ophthalmol 120:1707,2002)和抗凝血酶III(IOVS 44:332,2003)的神经保护作用以及抗LOX-1抗体通过抑制白细胞-内皮细胞相互作用对内毒素诱导的炎症的有益作用(ProNatl Acad Sci USA 100:1274,2003)。第三,我们证明了LEDGF(内源性和外源性存活因子)对视网膜损伤的神经保护作用(Brain Res 991:163,2003)。第四,我们阐明了与甲状腺素运载蛋白相关的家族性淀粉样多发性神经病相关的独特类型的继发性青光眼的治疗的临床和手术结果(Arch Ophthalmol 121:351,2003)。
项目成果
期刊论文数量(24)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Inomata Y, Hirata A, Yonemura N, Koga T, Kido N, Tanihara H: "Neuroprotective effects of interleukin-6 on NMDA-induced rat retinal damage"Biochem Biophys Res Commun. 302(2). 226-232 (2003)
Inomata Y、Hirata A、Yonemura N、Koga T、Kido N、Tanihara H:“白细胞介素 6 对 NMDA 诱导的大鼠视网膜损伤的神经保护作用”Biochem Biophys Res Commun。
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Honjo M, et al.: "Lectin-like oxidized LDL receptor-1 is a cell-adhesion molecule involved in endotoxin-induced inflammation."Proc Natl Acad Sci USA. 100. 1274-1279 (2003)
Honjo M 等人:“凝集素样氧化 LDL 受体 1 是一种参与内毒素诱导炎症的细胞粘附分子。”Proc Natl Acad Sci USA。
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Nishijima K, Kiryu J, Tsujikawa A, Honjo M, Nonaka A, Yamashiro K, Kamizuru H, Ieki Y, Tanihara H, Honda Y, Ogura Y: "Inhibitory effects of antithrombin III on interactions between blood cells and endothelial cells during retinal ischemia-reperfusion inju
Nishijima K、Kiryu J、Tsujikawa A、Honjo M、Nonaka A、Yamashiro K、Kamizuru H、Ieki Y、Tanihara H、Honda Y、Ogura Y:“抗凝血酶 III 对视网膜缺血期间血细胞和内皮细胞之间相互作用的抑制作用
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Inomata Y, Hirata A, Koga T, Kimura A, Singh DP, Shinohara T, Tanihara H: "Lens epithelium-derived growth factor : neuroprotection on rat retinal damage induced by N-methyl-D-aspartate"Brain Research. 991・1-2. 163-170 (2003)
Inomata Y、Hirata A、Koga T、Kimura A、Singh DP、筱原 T、Tanihara H:“晶状体上皮源性生长因子:N-甲基-D-天冬氨酸诱导的大鼠视网膜损伤的神经保护”脑研究 991・1。 -2。163-170(2003)
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Honjo M, Nakamura K, Yamashiro K, Kiryu J, Tanihara H, McEvoy LM, Honda Y, Butcher EC, Masaki T, Sawamura, T: "Lectin-like oxidized LDL receptor-1 is a cell-adhesion molecule involved in endotoxin-induced inflammation"Proc Natl Acad Sci U S A. 100・3. 1274
Honjo M、Nakamura K、Yamashiro K、Kiryu J、Tanihara H、McEvoy LM、Honda Y、Butcher EC、Masaki T、Sawamura、T:“凝集素样氧化 LDL 受体 1 是一种细胞粘附分子,参与内毒素-炎症诱发“Proc Natl Acad Sci U S A. 100・3. 1274
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TANIHARA Hidenobu其他文献
TANIHARA Hidenobu的其他文献
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{{ truncateString('TANIHARA Hidenobu', 18)}}的其他基金
Study on development of new therapeutic methods based on plasticity of trabecular meshwork cells
基于小梁网细胞可塑性开发新治疗方法的研究
- 批准号:
17K19729 - 财政年份:2017
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Challenging Research (Exploratory)
Investigation of glaucoma pathology focusing on epigenome and fibrocyte in aqueous humor dynamics and wound healing
青光眼病理学研究,重点关注房水动力学和伤口愈合中的表观基因组和纤维细胞
- 批准号:
17H04351 - 财政年份:2017
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
4-dimention live imaging of inflamatory cells in conjunctiva after glaucoma surgery
青光眼术后结膜炎症细胞的四维实时成像
- 批准号:
25670735 - 财政年份:2013
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Establishment of therapeutic assessment in glaucoma neuroprotection using live-imaging of axonal transport in optic nerve
利用视神经轴突运输的实时成像建立青光眼神经保护的治疗评估
- 批准号:
23659814 - 财政年份:2011
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
The effects of aqueous bioactive molecules on aqueous outflow dynamics and filtration-surgery results
水性生物活性分子对房水流出动力学和滤过手术结果的影响
- 批准号:
23390403 - 财政年份:2011
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
New therapeutic approach for glaucoma via drug-mediated bleb regulation
通过药物介导的滤泡调节治疗青光眼的新方法
- 批准号:
20390449 - 财政年份:2008
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
The investigation for molecular mechanisms of aqueous humor outflow and the creation of new treatments for intraocular pressure elevation in glaucomatous eyes
青光眼眼房水流出的分子机制研究及眼压升高新疗法的开发
- 批准号:
18390470 - 财政年份:2006
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
The development and clinical application of molecular-based new medical treatments for glaucoma
青光眼分子新疗法的开发及临床应用
- 批准号:
16390500 - 财政年份:2004
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Development of gene theropy for glaucoma by neaws of modulation of proteoglycan praduction in aqueous outflow rocite
通过调节房水流出液中蛋白多糖的产生来开发青光眼基因疗法
- 批准号:
08457464 - 财政年份:1996
- 资助金额:
$ 9.54万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
相似国自然基金
酸敏感离子通道功能与调控机理研究
- 批准号:30830035
- 批准年份:2008
- 资助金额:190.0 万元
- 项目类别:重点项目
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Dissecting the complex role of microglia states in glaucoma
剖析小胶质细胞状态在青光眼中的复杂作用
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Optineurin功能障碍通过一种新的分子机制诱导正常眼压青光眼的神经变性
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