Our results revealed that, compared with untreated diabetes, serum NO, MDA, and AGEs concentrations were downregulated and antioxidative SOD, GSH-Px, and CAT activities were upregulated by FSM, which indicated that FSM could protect the retinal structure and function via regulating nitrogen species homeostasis, reducing oxidative stress, and ameliorating inflammatory response. The gene discussed is SOD1; the disease is diabetes mellitus.