摘要Background Currently,no medicine is available that can prevent or treat neural damage associated with optic nerve injury.Minocycline is recently reported to have a neuroprotective function.The aims of this study were to exarmine the neuroprotective effect of minocycline on retinal ganglion cells (RGCs) and determine its underlying mechanisms,using a mouse model of optic nerve crush (ONC).Methods ONC was performed in the left eye of adult male mice,and the mice were randomly divided into minocycline-treated group and saline-treated control group.The mice without receiving ONC injury were used as positive controls.RGC densities were assessed in retinal whole mounts with immunofluorescence labeling of βⅢ-tubulin.Transmission electron microscopy was used to detect RGC morphologies,and Western blotting and real-time PCR were applied to investigate the expression of autophagy markers LC3-Ⅰ,LC3-Ⅱ,and transcriptional factors nuclear factor-κB1 (NF-κB1),NF-κB2.Results In the early stage after ONC (at Days 4 and 7),the density of RGCs in the minocycline-treated group was higher than that of the saline-treated group.Electron micrographs showed that minocycline prevented nuclei and mitochondria injuries at Day 4.Western blotting analysis demonstrated that the conversion of LC3-Ⅰ to LC3-Ⅱ was reduced in the minocycline-treated group at Days 4 and 7,which meant autophagy process was inhibited by minocycline.In addition,the gene expression of NF-κB2 was upregulated by minocycline at Day 4.Conclusion The neuroprotective effect of minocycline is generated in the early stage after ONC in mice,partly through delaying autophagy process and regulating NF-κB2 pathway.