背景目的：以光照誘發視網膜退化病變的動物模式來探討視網膜下腔移植臍帶間 質幹細胞可能的治療或視網膜保護功效。實驗方法：實驗以SD 大鼠為實驗動物，飼 養於光暗循環各12 小時的光照照度5000 到7000 lux 環境下7 天，以誘發視網膜退化 動物模式。光照完成後，移至正常光照之動物室繼續飼養，其中部分動物進行視網膜 下腔移植人類臍帶間質幹細胞，另一部分動物同部位注射生理食鹽水作為對照組。每 週以視網膜電位圖追蹤其視網膜功能變化，六週後取眼並進行視網膜組織切片以及免 疫螢光染色等實驗以研究不同組別之變化。結果：實驗結果顯示，光照一周後視網膜 感光細胞有明顯減少而視網膜電位圖亦顯示視網膜功能明顯退化。在視網膜下腔移植 人類臍帶間質幹細胞之後，感光細胞細胞有些為增家的趨勢，並且在三週後可以見到 有藍色螢光標記的移植細胞嵌入被移殖動物的視網膜內層組織中。視網膜電位圖的研 究結果也發現移植2 ～ 4 週之後，人類臍帶間質幹細胞移植的眼睛比對照組眼睛顯示 較佳的視網膜功能。免疫螢光染色的研究結果進一步發現，這些移植的幹細胞已經分 化為視網膜的色素上皮細胞（RPE）、穆勒膠細胞（Müller cells）、感光細胞（photoreceptor） 以及Amacrine細胞。同時SDF1α也有增加表現的趨勢。結論：研究結果顯示， 視網膜下腔移植人類臍帶間質幹細胞可能修復光照造成的視網膜感光細胞損傷並維持 或改善視網膜功能。此研究成果期望可做為臨床治療視網膜退化疾病之應用參考。

Background and Purpose: We used an animal model for light-induced retinal degeneration to investigate the possible therapeutic effect of transplanted umbilical cord mesenchymal stem cells (UMSC) in retina. Methods: Sprague-Dawley (SD) rats were exposed to cyclic, luminous light for 7 days, thereafter UMSCs were transplanted into the subretinal space. The effect was examined functionally by electroretinograph (ERG) before and after UMSC transplantation. Retinas were harvested for immunofluorescent and histological analyses to measure the changes of the outer nuclear layer (ONL) after transplantation. Results: Exposure to light for 7 days significantly reduced the amplitude of a- and b-waves of ERG, and decreased ONL thickness. After UMSC transplantation, the amplitude of a- and b-waves in UMSCtreated eyes was larger than that in the untreated eyes. The ONL of UMSC-treated retinas was thicker than that in the untreated eyes. Three weeks after transplantation, some of the grafted cells had migrated as single scattered cells into the ONL, the inner nuclear layer, and the ganglion cell layer. Grafted UMSCs were differentiated into several different retinal cells, including retinal pigmented epithelium cells, photoreceptors, amacrine cells, and horizontal cells, which were identified by retinal immunohistochemistry. Conclusion: These results demonstrate that transplantation of UMSCs improves both physiological retinal function and retinal morphology of light-induced retinopathy.