中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2004年
5期
998-1000
,共3页
刘学政%侯瑞鹏%萧鸿%李永洋%于树春
劉學政%侯瑞鵬%蕭鴻%李永洋%于樹春
류학정%후서붕%소홍%리영양%우수춘
视网膜%视细胞%光损伤%细胞凋亡
視網膜%視細胞%光損傷%細胞凋亡
시망막%시세포%광손상%세포조망
目的:研究视网膜光损伤与视细胞凋亡的相互关系,以探讨视网膜光损伤的发生发展机制.方法:所有SD大鼠经循环光环境适应7 d,实验前暗适应36 h,分别于光照3,6,9,12,15和18 h,灌流固定,摘除眼球.光镜标本在常规脱水、透明、石蜡包埋切片后,行苏木精-伊红(HE)、TUNEL法染色,光镜观察;电镜标本在树脂包埋、超薄切片、醋酸-柠檬酸铅双重染色后,透射电镜观察;应用CIAS-1 000图像分析系统定量检测外核层面积和视细胞凋亡指数,所得数据作统计学分析.结果:可见视网膜出现光损伤和视细胞凋亡现象,随着光照时间的延长,视网膜光损伤逐渐加重,视细胞凋亡逐渐增多.在外核层,透射电镜观察见核染色质浓集,而无炎性反应.外核层面积和视细胞凋亡指数作相关性分析有显著意义.结论:视细胞凋亡是视网膜光损伤的重要机制;光损伤启动了视细胞凋亡的发生,外核层细胞核的丢失是视细胞凋亡的结果;视网膜光损伤与视细胞凋亡有着密不可分的联系.
目的:研究視網膜光損傷與視細胞凋亡的相互關繫,以探討視網膜光損傷的髮生髮展機製.方法:所有SD大鼠經循環光環境適應7 d,實驗前暗適應36 h,分彆于光照3,6,9,12,15和18 h,灌流固定,摘除眼毬.光鏡標本在常規脫水、透明、石蠟包埋切片後,行囌木精-伊紅(HE)、TUNEL法染色,光鏡觀察;電鏡標本在樹脂包埋、超薄切片、醋痠-檸檬痠鉛雙重染色後,透射電鏡觀察;應用CIAS-1 000圖像分析繫統定量檢測外覈層麵積和視細胞凋亡指數,所得數據作統計學分析.結果:可見視網膜齣現光損傷和視細胞凋亡現象,隨著光照時間的延長,視網膜光損傷逐漸加重,視細胞凋亡逐漸增多.在外覈層,透射電鏡觀察見覈染色質濃集,而無炎性反應.外覈層麵積和視細胞凋亡指數作相關性分析有顯著意義.結論:視細胞凋亡是視網膜光損傷的重要機製;光損傷啟動瞭視細胞凋亡的髮生,外覈層細胞覈的丟失是視細胞凋亡的結果;視網膜光損傷與視細胞凋亡有著密不可分的聯繫.
목적:연구시망막광손상여시세포조망적상호관계,이탐토시망막광손상적발생발전궤제.방법:소유SD대서경순배광배경괄응7 d,실험전암괄응36 h,분별우광조3,6,9,12,15화18 h,관류고정,적제안구.광경표본재상규탈수、투명、석사포매절편후,행소목정-이홍(HE)、TUNEL법염색,광경관찰;전경표본재수지포매、초박절편、작산-저몽산연쌍중염색후,투사전경관찰;응용CIAS-1 000도상분석계통정량검측외핵층면적화시세포조망지수,소득수거작통계학분석.결과:가견시망막출현광손상화시세포조망현상,수착광조시간적연장,시망막광손상축점가중,시세포조망축점증다.재외핵층,투사전경관찰견핵염색질농집,이무염성반응.외핵층면적화시세포조망지수작상관성분석유현저의의.결론:시세포조망시시망막광손상적중요궤제;광손상계동료시세포조망적발생,외핵층세포핵적주실시시세포조망적결과;시망막광손상여시세포조망유착밀불가분적련계.
AIM: To observe the relationship between retinal photic injury and receptor cell apoptosis, exploring the development mechanism of retinal photic injury. METHODS: SD rats were maintained under a cyclic light/dark environment for 7 days and then kept in darkness for 36 hours before experiment. The rats were sacrificed after continuous intense white light exposure for 3, 6, 9, 12, 15, and 18 hours. Light microscopy samples were enucleated and fixed after perfusion, then processed and embedded in paraffin using routine procedures. All sections for examination under light microscopy were made by Haematine-Eosin(HE) and TUNEL staining. Sections prepared for electron microscopy were embedded in colophony, then they were sliced into ultrathin sections and dyed by acetate-citric lead. The outer nuclear layer area and cell apoptosis index were quantified using the CIAS-1 000 cell photo analysis system, and the data were statistically analyzed. RESULTS: Photic injury and receptor cell apoptosis were found in the retina. Photic injury in the retina worsened and optic cell apoptosis increased as time of light exposure increased. Condensation of chromatin did not reveal any inflamatory response under electron microscopy. The relationship between outer nuclear layer area(OA) and the apoptosis index (AI) was compared using relative analysis. There were significant differences between them.CONCLUSION: Apoptosis is an important mechanism in light-induced retinal damage. Light triggers the apoptosis of photoreceptor cells. The loss of cells in OA is the result of apoptosis. Photic injury closely correlated to receptor cell apoptosis.