CAJ | 학술논문

目的探讨活化的巨噬细胞在视神经损伤修复中的作用.方法选取112只健康新西兰大耳白兔作为实验动物,按随机数字表法随机分为实验组和对照组,每组各56只,按照不同观察时间点(1、4、7、10、14、21、28 d)每组分为7个亚组,每亚组8只.用液压冲击颅脑损伤仪(FPI)建立外伤性视神经不完全损伤联合晶体损伤模型作为实验组,外伤性视神经不完全损伤模型作为对照组.应用闪光视觉诱发电位(FVEP)分析并比较实验组、对照组建模前及建模后不同时间点视神经功能变化情况,组织病理学方法观察并比较实验组、对照组建模后视网膜组织中巨噬细胞及神经节细胞变化情况.结果建模前,实验组FVEP P100波潜伏时为(42.74±5.83)ms,振幅为(7.98±2.15)μV.建模后1 d,实验组FVEP P100波潜伏时为(103.91±10.89)ms,较建模前延长,差异有统计学意义(t=-8.464,P=0.000);振幅(6.39±2.19)μV,较建模前降低,差异有统计学意义(t=-2.094,P=0.000).建模后10 d,实验组P100波潜伏时最长,之后逐渐恢复(F=35.894,P=0.000).建模后7 d,实验组P100波振幅最低,之后逐渐回升(F=6.594,P=0.000).组织病理学检查显示,建模后1 d,实验组视网膜、视神经未见活化的巨噬细胞,之后逐渐增多,10 d时到达高峰(91.25±6.91),之后又逐渐减少,差异有统计学意义(F=21.277,P=0.000);建模后1 d,实验组视网膜未出现神经节细胞轴突再生,7 d时出现,平均值为6.38±1.85,之后逐渐增多,28 d时到达高峰,平均值为49.63±2.50,差异有统计学意义(F=7.711,P=0.000).结论视神经不完全损伤联合晶状体损伤后,视神经可逐渐修复,活化的巨噬细胞在视神经不完全损伤修复中起着重要的作用.
목적 탐토활화적거서세포재시신경손상수복중적작용.방법 선취112지건강신서란대이백토작위실험동물,안수궤수자표법수궤분위실험조화대조조,매조각56지,안조불동관찰시간점(1、4、7、10、14、21、28 d)매조분위7개아조,매아조8지.용액압충격로뇌손상의(FPI)건립외상성시신경불완전손상연합정체손상모형작위실험조,외상성시신경불완전손상모형작위대조조.응용섬광시각유발전위(FVEP)분석병비교실험조、대조조건모전급건모후불동시간점시신경공능변화정황,조직병이학방법 관찰병비교실험조、대조조건모후시망막조직중거서세포급신경절세포변화정황.결과 건모전,실험조FVEP P100파잠복시위(42.74±5.83)ms,진폭위(7.98±2.15)μV.건모후1 d,실험조FVEP P100파잠복시위(103.91±10.89)ms,교건모전연장,차이유통계학의의(t=-8.464,P=0.000);진폭(6.39±2.19)μV,교건모전강저,차이유통계학의의(t=-2.094,P=0.000).건모후10 d,실험조P100파잠복시최장,지후축점회복(F=35.894,P=0.000).건모후7 d,실험조P100파진폭최저,지후축점회승(F=6.594,P=0.000).조직병이학검사현시,건모후1 d,실험조시망막、시신경미견활화적거서세포,지후축점증다,10 d시도체고봉(91.25±6.91),지후우축점감소,차이유통계학의의(F=21.277,P=0.000);건모후1 d,실험조시망막미출현신경절세포축돌재생,7 d시출현,평균치위6.38±1.85,지후축점증다,28 d시도체고봉,평균치위49.63±2.50,차이유통계학의의(F=7.711,P=0.000).결론 시신경불완전손상연합정상체손상후,시신경가축점수복,활화적거서세포재시신경불완전손상수복중기착중요적작용.
Objective To explore the role of activated macrophage in the repair of traumatic optic nerve injury in an animal model of incomplete traumatic optic nerve injury with lens damage. Methods One hundred and twelve healthy New Zealand big ear white rabbits were divided into two groups (experimentaland control groups) randomly. According to the different time points (one, four, seven, ten, 14, 21 and 28 days), each group was further divided into seven subgroups, each subgroup had eight rabbits. Traumatic optic neuropathy and lens damage were induced in one eye of each rabbit by fluid percussion brain injury device (FPI);those eyes were the experimental group. The eyes of control group only had traumatic optic neuropathy. The functional and morphological changes of retina and optic nerve were evaluated by histopathology and flash-visual evoked potential (FVEP). Results FVEP P100 latency was (42.74± 5.83)ms, P100 amplitude was (7.98 ± 2.15) μV before optic nerve injury was induced. One day after the injury,the P100 latency increased and the P100 amplitude reduced significantly. The P100 latency reached the longest at ten days after injury, and then recovered gradually. The P100 amplitude reached the lowest at seven days after injury, and then recovered gradually. The histopathological examination showed activated macrophages were not detected in the retina and optic nerve at day one after the injury, then they increased gradually and reached their peak (91.25 ±-6.91) at day ten, and decreased after that, the difference was statistically significant (F= 21. 277, P= 0. 000);retinal ganglion cell axon regeneration began at day seven after the injury with an average of (6.38± 1.85). The axons increased gradually and reached their peak (49.63±2. 50) at day 28, and the changes were significant (F=7. 711, P=0. 000). Conclusions Incomplete optic nerve injury can recover gradually if there is lens damage at the same time. Activated macrophage may playan important role in this recovery process.