Cordyceps cicadae mycelium is an herbal medicine used to provide anti-inflammatory and antiapoptotic actions. However, little is known about the role of C. cicadae mycelium in neuroprotection. This study aimed to investigate the neuroprotective effects of C. cicadae mycelium extract (CCME) in the optic nerve crush (ONC) model. The optic nerves of adult male Wistar rats (aged 7-8 weeks) were crushed by a standardized method. Rats were divided equally into three groups: 1) a sham-operated group (sham), 2) a phosphate buffered saline-treated control group (crush), and 3) a CCME-treated group (CCME) that received CCME once daily for 7 consecutive days at doses of 100 mg/kg before ONC. Two weeks after ONC in rats, retinal ganglion cell (RGC) density and visual function were determined by using retrograde labeling with FluoroGold and flash visual evoked potentials. The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and immunohistochemistry of ED1 (a marker of macrophage/microglia) were used to evaluate the antiapoptotic and anti-inflammatory effects of CCME in the optic nerve section. The P1-N2 amplitude and RGC density in the CCME-treated group were higher than those in the ONC control (crush) group by 5.15- and 3.13-fold, respectively. The numbers of TUNEL-positive cells and ED1-positive cells in the CCME-treated group were reduced by 4.38- and 6.63-fold, respectively, compared to those in the crush group. Oral administration of CCME provided neuroprotective effects in the ONC model via antiapoptotic and anti-inflammatory actions, which provides a potential treatment for patient with traumatic optic neuropathy.