The role of activated macrophage in the repair of traumatic optic nerve injury

Abstract

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. Key words: Optic nerve injuries; Macrophages; Animal experimentation