中华眼科杂志
中華眼科雜誌
중화안과잡지
Chinese Journal of Ophthalmology
2010年
12期
1084-1089
,共6页
张蔚%于金国%王兴%申占省%张静楷%颜华
張蔚%于金國%王興%申佔省%張靜楷%顏華
장위%우금국%왕흥%신점성%장정해%안화
视神经损伤%半胱氨酸天冬氨酸蛋白酶3%寡肽类%视网膜神经节细胞%免疫%组织化学
視神經損傷%半胱氨痠天鼕氨痠蛋白酶3%寡肽類%視網膜神經節細胞%免疫%組織化學
시신경손상%반광안산천동안산단백매3%과태류%시망막신경절세포%면역%조직화학
Optic nerve injuries%Caspase3%Oligopeptides%Retinal ganglion cells%Immunohistochemistry
目的 观察半胱氨酸天冬氨酸蛋白酶3(Caspase-3)抑制剂z-DEVD-fmk对兔外伤性视神经损伤的治疗效果.方法 实验研究.选取2～3月龄中国白兔52只(104只眼),4只(8只眼)作为空白对照,48只(96只眼)应用液压冲击颅脑损伤仪建立兔外伤性视神经损伤模型,左眼玻璃体腔注射2%二甲基亚砜5μl为对照组(A组);右眼玻璃体腔注射Capase-3抑制剂z-DEVD-fmk 5μl为实验组(B组).给药后1 d、4 d、7 d、10 d、14 d、21 d行闪光视觉诱发电位(F-VEP),视网膜病理学检查,并应用免疫组织化学方法检测视网膜中Caspase-3表达.所得数据采用t检验、单因素方差分析、q检验及直线相关分析进行统计学处理.结果 给药后7 d,实验组的F-VEP P1波潜伏(90.50±7.61)ms与对照组(113.59±12.92)ms相比缩短(t=4.060,P＜0.05),视网膜神经节细胞计数实验组(237.62±8.50)较对照组(207.03±11.04)有所增多(t=-5.843,P＜0.05),均可持续至给药后21 d,实验组的F-VEP P1波潜伏(67.97±7.93)ms与对照组(134.22±8.50)ms相比缩短(t=13.950,P＜0.05);视网膜神经节细胞计数实验组(207.13±12.21)较对照组(156.32±8.45)增多(t=-10.307,P＜0.05).Caspase-3的A值于给药后7 d,实验组(0.396±0.023)低于对照组(0.458±0.024),差异有统计学意义(t=6.200,P＜0.05).F-VEP P1波潜伏期与Caspase-3 A值呈正相关(r=0.95,P＜0.05).结论 z-DEVD-fmk通过抑制视网膜Caspase-3的表达,对兔外伤性视神经损伤具有治疗作用,可促进神经功能的恢复.
目的 觀察半胱氨痠天鼕氨痠蛋白酶3(Caspase-3)抑製劑z-DEVD-fmk對兔外傷性視神經損傷的治療效果.方法 實驗研究.選取2～3月齡中國白兔52隻(104隻眼),4隻(8隻眼)作為空白對照,48隻(96隻眼)應用液壓遲擊顱腦損傷儀建立兔外傷性視神經損傷模型,左眼玻璃體腔註射2%二甲基亞砜5μl為對照組(A組);右眼玻璃體腔註射Capase-3抑製劑z-DEVD-fmk 5μl為實驗組(B組).給藥後1 d、4 d、7 d、10 d、14 d、21 d行閃光視覺誘髮電位(F-VEP),視網膜病理學檢查,併應用免疫組織化學方法檢測視網膜中Caspase-3錶達.所得數據採用t檢驗、單因素方差分析、q檢驗及直線相關分析進行統計學處理.結果 給藥後7 d,實驗組的F-VEP P1波潛伏(90.50±7.61)ms與對照組(113.59±12.92)ms相比縮短(t=4.060,P＜0.05),視網膜神經節細胞計數實驗組(237.62±8.50)較對照組(207.03±11.04)有所增多(t=-5.843,P＜0.05),均可持續至給藥後21 d,實驗組的F-VEP P1波潛伏(67.97±7.93)ms與對照組(134.22±8.50)ms相比縮短(t=13.950,P＜0.05);視網膜神經節細胞計數實驗組(207.13±12.21)較對照組(156.32±8.45)增多(t=-10.307,P＜0.05).Caspase-3的A值于給藥後7 d,實驗組(0.396±0.023)低于對照組(0.458±0.024),差異有統計學意義(t=6.200,P＜0.05).F-VEP P1波潛伏期與Caspase-3 A值呈正相關(r=0.95,P＜0.05).結論 z-DEVD-fmk通過抑製視網膜Caspase-3的錶達,對兔外傷性視神經損傷具有治療作用,可促進神經功能的恢複.
목적 관찰반광안산천동안산단백매3(Caspase-3)억제제z-DEVD-fmk대토외상성시신경손상적치료효과.방법 실험연구.선취2～3월령중국백토52지(104지안),4지(8지안)작위공백대조,48지(96지안)응용액압충격로뇌손상의건립토외상성시신경손상모형,좌안파리체강주사2%이갑기아풍5μl위대조조(A조);우안파리체강주사Capase-3억제제z-DEVD-fmk 5μl위실험조(B조).급약후1 d、4 d、7 d、10 d、14 d、21 d행섬광시각유발전위(F-VEP),시망막병이학검사,병응용면역조직화학방법검측시망막중Caspase-3표체.소득수거채용t검험、단인소방차분석、q검험급직선상관분석진행통계학처리.결과 급약후7 d,실험조적F-VEP P1파잠복(90.50±7.61)ms여대조조(113.59±12.92)ms상비축단(t=4.060,P＜0.05),시망막신경절세포계수실험조(237.62±8.50)교대조조(207.03±11.04)유소증다(t=-5.843,P＜0.05),균가지속지급약후21 d,실험조적F-VEP P1파잠복(67.97±7.93)ms여대조조(134.22±8.50)ms상비축단(t=13.950,P＜0.05);시망막신경절세포계수실험조(207.13±12.21)교대조조(156.32±8.45)증다(t=-10.307,P＜0.05).Caspase-3적A치우급약후7 d,실험조(0.396±0.023)저우대조조(0.458±0.024),차이유통계학의의(t=6.200,P＜0.05).F-VEP P1파잠복기여Caspase-3 A치정정상관(r=0.95,P＜0.05).결론 z-DEVD-fmk통과억제시망막Caspase-3적표체,대토외상성시신경손상구유치료작용,가촉진신경공능적회복.
Objective To observe the effects of caspase-3 inhibitor z-DEVD-fmk on optic nerve injury of rabbits. Methods It was an experimental study. Two to three month-old rabbits were used in this study. The rabbit model of optic nerve injury was created by fluid percussion brain injury device (FPI).DMSO (5μl 2% solution) was injected intravitreally to the left eyes (control group). Caspase-3 inhibitor z-DEVD-fmk (5 μl) was injected intravitreally to the right eyes (experimental group). Flash-visual evoked potential (F-VEP) and histopathological examination of the retina were used to check the variations in optic nerve injury at 1,4, 7, 10, 14, and 21 days after the treatment. Immunohistochemistry was used to detect the expression of caspase-3 in the retina. T-test, variance analysis, q-test and linear correlation analysis were used to analyze these data. Results At the 7th day after treatment, the latency of F-VEP P1 in experimental group was shorter than that in the control group [(90.50 ± 7.61 ) ms vs (113.59 ±12. 92) ms, t = 4. 060, P ＜ 0. 05]and the number of retinal ganglion cells (RGC) in the experimental group was greater than that in the control group ( 237. 62 ± 8. 50 vs 207. 03 ± 11. 04, t = - 5. 843, P ＜0. 05). Both of these trends continued to the 21st day after treatment [(67.97 ±7.93) ms vs. ( 134. 22 ±8.50) ms, t=13.950, P＜0. 05; 156.32±8.45 vs. 207.13±12.21, t= -10.307, P＜0. 05]. The absorbency (A) of caspase-3 in the experimental group (0. 396 ±0. 023) was lower than that in the control group (0. 458 ± 0. 024 ) and this difference was statistically significant ( t= 6. 200, P ＜ 0. 05 ) at the 7th day after treatment. The latency of F-VEP P1 and the absorbency of caspase-3 in the retina were positively correlated with each other(r=0. 95,P＜0. 05). Conclusion z-DEVD-fmk is effective in treating rabbit optic nerve injury by inhibiting the expression of caspase-3 in the retina. It can promote the recovery of optic nerve function.
