This series of experiments strongly indicated that OSSCE mediates the protection against retinal apoptosis resulting from hyperglycaemia by simultaneously modulating AGE levels, oxidative stress-induced retinal apoptosis, and mitochondrial dysfunction through the inhibition of NF-κB translocation into the nucleus via the downregulation of PKCδ, P47phox subunit of NADPH oxidase, and ERK1/2, although OSSCE, itself, could not properly control the levels of blood glucose and HbA1c in SDT rats. The gene discussed is FMO5; the disease is Hyperglycemia.