廖嘉鴻董耀中2026-05-122026-05-122010-06-23https://203.71.86.71/handle/123456789/13326學位別：博士 語文別：英文 指導教授：廖嘉鴻 共同指導教授： 口試委員：林山陽;周玉山;張淑芬;蔡郁惠 中文關鍵字：聚合微胞體;角膜細胞凋亡Corneal epithelial damages cause stromal keratocyte apoptosis and excessive keratocyte apoptosis is associated with the pathologic mechanisms of corneal changes seen in corneal disorders. Scraping of corneal epithelium (debridement), an epithelial damage, yields keratocyte apoptosis including DNA fragmentation and cellular morphological changes in the anterior stroma underlying the injured epithelium. In the study, activation of caspase-3 and reduction of bcl-xL were detected in cornea after corneal epithelial debridement except for DNA fragmentation and cellular morphological changes. We delivered the plasmid encoding an anti-apoptotic gene, Bcl-xL (pCMV-bcl-xL-eGFP) with polymeric micelle (PM) via eye drop to epithelial debridement cornea. After six doses of eye drop within 48 hr, mRNA of bcl-xL was significantly increased at 48 hr (2.2-fold, P< 0.05) and mRNA of eGFP was detected at 48 hr (4571.7 ± 1194.5 copies/ug total RNA). The bcl-xL-eGFP fusion protein was detected in wounded cornea. Furthermore, both DNA fragmentation and caspase-3 activity were significantly decreased (61% at 48 hr, P< 0.05) in epithelial debridement cornea with eye drop of pCMV-bcl-xL-eGFP/PM. Thus, eye drop of pCMV-bcl-xL-eGFP/PM reduced apoptosis for corneal epithelial damage.系所名稱：藥學系(博士班)thesis