RESUMO
Objective To investigate the effect of α-crystallin on the proliferation of rat retinal microglia after optic nerve injury. Methods The effect of α-crystallin on number and proliferation of microglia were analyzed by MTT assay.After the rat model with optic nerve injury was established,α-crystallin was iniected into vitreous cavity and the microglia cell number were counted and compared by retinal fiat counting and immunofluorescence labeling in different groups. Results The proliferation and activation of microglia cells could be stimulated by LPS at 10-6g/L to 10-2g/L.α-crystallin at 10-4g/L and 10-6g/L could inhibit proliferation and activation of microglia cells.Compared to BSA iniection group,α-crystallin could inhibit more significantly the number of microglia cells 1-3 weeks after injury (P＜0.05). Conclusions α-crystallin can inhibit proliferation and activation of retinal microglia and alleviate overphagocytosis and secondary damage of retinal microglia to retinal ganglion cells(RGCs),which may be another mechanism that α-crystallin contributes to indirect protection of RGCs.
RESUMO
Objective To create a calibrated animal model of graded optic nerve injury (ONI) in rats, focusing on quantification of injury intensity, injury severity and the correlation between them. Methods A pair of cross-action forceps with pressure of 148.0 g was used to clip rat optic nerves for 3, 6, 30 and 60 seconds, or a pair of artery clips with constant pressure (32.4 g) used to clip rat optic nerves for 5, 10 and 15 seconds in order to create graded ONI animal models. Transcranial FluoroGold-labeled retinal ganglion cell (RGC) was used to observe the changes of RGC one month after injury, which then could be used to evaluate the injury severity. Ocular blood supply was evaluated by transcardiacly perfused Luxol Fast Blue post-injury. Results The graded ONI animal models were successfully created in rats without retinal ischemia post-trauma. The injury intensity could be well-defined by impulse or averaged impulse, while injury severity could be evaluated by the count of FluoroGold-labeled RGCs. The averaged impulse produced by artery clips clipping rat optic nerves for 15 seconds equalized with that produced by cross-action forceps for three seconds. The severer injury intensity begot less number of RGCs. The correlation between injury impulse and RGCs was fit for power function. Short time clipping of optic nerves could not lead to ischemic injury of the retina. Conclusions A calibrated graded ONI animal model is successfully created by clipping optic nerves with a pair of cross-action forceps. The model can be evaluated with RGCs count, impulse and averaged impulse, the latter two of which stand for injury intensity and injury severity, respectively.