眼科研究
眼科研究
안과연구
CHINESE OPHTHALMIC RESEARCH
2010年
3期
203-206
,共4页
范芳%林宏华%葛正龙%刘华庆%曾小平%蔡善君%李海祥
範芳%林宏華%葛正龍%劉華慶%曾小平%蔡善君%李海祥
범방%림굉화%갈정룡%류화경%증소평%채선군%리해상
c-myc反义寡核苷酸%半乳糖%白内障%细胞凋亡
c-myc反義寡覈苷痠%半乳糖%白內障%細胞凋亡
c-myc반의과핵감산%반유당%백내장%세포조망
c-myc antisense oligodeoxynucleotide%galactose%cataract%cell apoptosis
目的 研究c-myc反义寡核苷酸(ASODN)对半乳糖性白内障晶状体上皮细胞(LECs)凋亡的影响.方法 将Wistar大鼠按随机数字表法分为生理盐水组、半乳糖组和半乳糖+c-myc ASODN组,每组36只.半乳糖组及半乳糖+c-myc ASODN组每日球后注射0.2mL 20%半乳糖,制作大鼠半乳糖性白内障模型,半乳糖+c-myc ASODN组球后注射半乳糖4h后加注Lipo-c-myc ASODN复合液0.2mL,隔日1次.分别于给药后7、14、24d处死动物,取出晶状体,检测LECs的凋亡情况,采用TUNEL法检测c-myc ASODN对半乳糖诱导LECs凋亡的影响,透射电镜下观察LECs超微结构的改变.结果 各组在7、14、24d的LECs凋亡率比较,差异均有统计学意义(F_(7 days)=3418.495,P＜0.01;F_(14 days)=1137.555,P＜0.01;F_(24 days)=2198.871,P＜0.01);24d时半乳糖组LECs的凋亡率为56.57±3.20,生理盐水组为0.37±0.11,差异有统计学意义(P＜0.01);半乳糖+c-myc ASODN组细胞凋亡率为29.35±1.63,较半乳糖组明显降低(P＜0.05).透射电镜下观察发现,半乳糖组可见LECs呈凋亡细胞的早期改变;随着高糖诱导时间的延长,凋亡细胞逐渐增多;生理盐水组几乎未见到凋亡细胞;半乳糖+c-myc ASODN组凋亡细胞数量较同期半乳糖组少.结论 在白内障形成过程中半乳糖能诱导LECs凋亡,c-myc ASODN能够抑制半乳糖诱导的LECs凋亡.
目的 研究c-myc反義寡覈苷痠(ASODN)對半乳糖性白內障晶狀體上皮細胞(LECs)凋亡的影響.方法 將Wistar大鼠按隨機數字錶法分為生理鹽水組、半乳糖組和半乳糖+c-myc ASODN組,每組36隻.半乳糖組及半乳糖+c-myc ASODN組每日毬後註射0.2mL 20%半乳糖,製作大鼠半乳糖性白內障模型,半乳糖+c-myc ASODN組毬後註射半乳糖4h後加註Lipo-c-myc ASODN複閤液0.2mL,隔日1次.分彆于給藥後7、14、24d處死動物,取齣晶狀體,檢測LECs的凋亡情況,採用TUNEL法檢測c-myc ASODN對半乳糖誘導LECs凋亡的影響,透射電鏡下觀察LECs超微結構的改變.結果 各組在7、14、24d的LECs凋亡率比較,差異均有統計學意義(F_(7 days)=3418.495,P＜0.01;F_(14 days)=1137.555,P＜0.01;F_(24 days)=2198.871,P＜0.01);24d時半乳糖組LECs的凋亡率為56.57±3.20,生理鹽水組為0.37±0.11,差異有統計學意義(P＜0.01);半乳糖+c-myc ASODN組細胞凋亡率為29.35±1.63,較半乳糖組明顯降低(P＜0.05).透射電鏡下觀察髮現,半乳糖組可見LECs呈凋亡細胞的早期改變;隨著高糖誘導時間的延長,凋亡細胞逐漸增多;生理鹽水組幾乎未見到凋亡細胞;半乳糖+c-myc ASODN組凋亡細胞數量較同期半乳糖組少.結論 在白內障形成過程中半乳糖能誘導LECs凋亡,c-myc ASODN能夠抑製半乳糖誘導的LECs凋亡.
목적 연구c-myc반의과핵감산(ASODN)대반유당성백내장정상체상피세포(LECs)조망적영향.방법 장Wistar대서안수궤수자표법분위생리염수조、반유당조화반유당+c-myc ASODN조,매조36지.반유당조급반유당+c-myc ASODN조매일구후주사0.2mL 20%반유당,제작대서반유당성백내장모형,반유당+c-myc ASODN조구후주사반유당4h후가주Lipo-c-myc ASODN복합액0.2mL,격일1차.분별우급약후7、14、24d처사동물,취출정상체,검측LECs적조망정황,채용TUNEL법검측c-myc ASODN대반유당유도LECs조망적영향,투사전경하관찰LECs초미결구적개변.결과 각조재7、14、24d적LECs조망솔비교,차이균유통계학의의(F_(7 days)=3418.495,P＜0.01;F_(14 days)=1137.555,P＜0.01;F_(24 days)=2198.871,P＜0.01);24d시반유당조LECs적조망솔위56.57±3.20,생리염수조위0.37±0.11,차이유통계학의의(P＜0.01);반유당+c-myc ASODN조세포조망솔위29.35±1.63,교반유당조명현강저(P＜0.05).투사전경하관찰발현,반유당조가견LECs정조망세포적조기개변;수착고당유도시간적연장,조망세포축점증다;생리염수조궤호미견도조망세포;반유당+c-myc ASODN조조망세포수량교동기반유당조소.결론 재백내장형성과정중반유당능유도LECs조망,c-myc ASODN능구억제반유당유도적LECs조망.
Background Various studies demonstrated that the apoptosis of lens epithelial cells(LECs) is associated with the overexpression of the c-myc gene in LECs induced by galactose.Inhibiting the abnormal expression of the c-myc gene in LECs is an effective approach to mitigate the pathogenesis and development of cataract.Objective The goal of this study is to investigate the inhibitory effects of c-myc antisense oligodeoxynucleotide(c-myc ASODN) on the apoptosis of LECs in the eye with galactose-induced cataract.Methods Galactose-induced cataract models were established by the retrobulbar injection of 0.2 mL of 20% galactose once per day.Lipo-antisense oligodeoxynucleotide(Lipo-ASODN,0.2 mL) was retrobulbarly injected 4 hours after the injection of galactose at one-day intervals.The animals were sacrificed and lenses were obtained to evaluate the apoptosis of LECs and the effect of c-myc ASODN on LECs apoptosis induced by galactose was examined by TUNEL assay after 7,14 and 24 days.The ultrastructural changes of LECs were examined under the transmission electron microscopy(TEM).Results A significant difference in the apoptotic rate of LECs was found among the 7 day,14 day and 24 day groups(F_(7 days)=3 418.495,P＜0.01;F_(14 days)=1137.555,P＜0.01;F_(24 days)=2198.871,P＜0.01).The apoptotic rate of LECs in the galactose group was markedly higher than that in the normal saline solution group 7 days,14 days and 24 days after the experiment(P＜0.01).The apoptotic rate of LECs in the galactose+lipo+ ASODN group significantly declined in comparison to the galactose group after 7 days,14 days and 24 days(P＜0.05).TUNEL assay showed the condensation,breakage and irregularity of the nuclei of apoptotic cells in the galactose group.The destruction of the ultrastructure of the cells and organelles were observed under the transmission electron microscope.Conclusion Galactose induces apoptosis of LECs in cataractogenesis.C-myc ASODN inhibits apoptosis of LECs induced by galactose.
