https://scholars.lib.ntu.edu.tw/handle/123456789/199816
Title: | 行政院國家科學委員會專題研究計畫期中進度報告:細胞間素活化轉錄因子 NF-KB 引起眼球內炎性反應的研究(2/3) | Authors: | 楊長豪 | Issue Date: | 2000 | Publisher: | 臺北市:國立臺灣大學醫學院眼科 | Abstract: | Purpose. To demonstrate the expression and location of fractalkine and receptor, CX3CR1, in iris/ciliary body and thus establish their roles in experimental autoimmune anterior uveitis, an animal model of human acute anterior uveitis. Methods. Uveitis was induced with the injection of melanin-associated antigen intraperitoneally and into the left footpad simultaneously. Some rats were treated with a putative NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC; 40 mg/kg/day) every day after immunization. At defined time points, fractalkine and CX3CR1 mRNA expression were semiquantified by using RT-PCR. Fractalkine in aqueous humor was determined by ELISA. The cellular sources of fractalkine were determined by immunhistochemical staining. Results. Fractalkine mRNA was found to be upregulated in iris/ciliary body 9 days after immunization, preceding clinical disease onset. CX3CR1 mRNA exhibited peak levels at day 14, coincident with disease onset. Fractalkine in aqueous humor showed a similar expression profile to mRNA expression. PDTC markedly inhibited the expression of fractalkine mRNA in iris/ciliary body and fractalkine protein in aqueous humor. Immuhistochemical staining revealed fractalkine was prominently expressed on vascular endothelial cells. Conclusions. This study was the first to provide evidences of fractalkine –CX3CR1 3 interactions in the genesis of experimental autoimmune anterior uveitis. The activation of fractalkine gene is, at least in part, via a NF-κB-dependent pathway. Therefore, selective anti-fractalkine or anti- NF-κB therapy may become a therapeutic potential for acute anterior uveitis treatment. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/29904 | Other Identifiers: | 892314B002035M47 | Rights: | 國立臺灣大學醫學院眼科 |
Appears in Collections: | 醫學系 |
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892314B002035M47.pdf | 117.45 kB | Adobe PDF | View/Open |
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