Impaired vision with oligemic ophthalmopathy is a result of excitotoxicity caused by excitatory amino acids, resulting in pathological changes, such as loss of retinal neurons and in particular retinal ganglionic cells. The present study utilized infant guinea pigs, aged 45-50 days, to establish injury models via intraperitoneal injection of fixed sodium glutamate doses. Results from hematoxylin- eosin staining revealed significantly reduced retinal ganglionic cell numbers and retinal damage at 10 days after 7 consecutive days of 3 g/kg sodium glutamate treatment; these animals served as the injury model group. In addition, models of moderate injury (glutamate 3 g/kg daily, for 7 consecutive days) were intraperitoneally pretreated with basic fibroblast growth factor (800 U/kg daily). Immunohistochemistry results confirmed reduced anti-apoptotic gene bcl-2 expression in the ganglion cell layer of glutamate-injured guinea pigs. Expression of the pro-apoptotic gene caspase-3 was increased in the ganglion cell layer and inner plexiform layer. Somatostatin expression was primarily distributed in the ganglion cell layer and inner nuclear layer. Expression of the presynaptic element synaptophysin was weak. However, following basic fibroblast growth factor injection, expressions of the above-described bioactive molecules were reversed, which suggested that basic fibroblast growth factor exerted protective effects on sodium glutamate-induced retinal injury in infant guinea pigs by regulating expression of synaptophysin, somatostatin, Bcl-2, and caspase-3. Impaired vision with oligemic ophthalmopathy is a result of excitotoxicity caused by excitatory amino acids, resulting in pathological changes, such as loss of retinal neurons and in particular retinal ganglionic cells. The present study of infant guinea pigs, aged 45-50 days, to establish injury models via intramatoidyl injection-fixed sodium glutamate doses. Results from hematoxylin-eosin TIP showed significantly reduced retinal ganglionic cell numbers and retinal damage at 10 days after 3 consecutive days of 3 g / kg sodium glutamate treatment; these animals served as the injury model In addition, models of moderate injury (glutamate 3 g / kg daily, for 7 consecutive days) were intraperitoneally pretreated with basic fibroblast growth factor (800 U / kg daily). Immunohistochemistry confirmed confirmed anti-apoptotic gene bcl-2 expression in the ganglion cell layer of glutamate-injured guinea pigs. Expression of the pro-apoptotic gene caspase-3 was increased in the ganglion cell layer and inner plexiform layer. Somatostatin expression was initially distributed in the ganglion cell layer and inner nuclear layer. Expression of the presynaptic element synaptophysin was weak. However, the following basic fibroblast growth factor injection, expressions of the above-described bioactive The molecules that have that induced that basic fibroblast growth factor exerted protective effects on sodium glutamate-induced retinal injury in infant guinea pigs by regulating expression of synaptophysin, somatostatin, Bcl-2, and caspase-3.