Effect of taxifolin on development of retinopathy in alloxan-induced diabetic rats.

Diabetic retinopathy (DR) is one of the leading causes of blindness. In DR patients, antioxidant defence is disrupted, and production of reactive oxygen species and pro-inflammatory cytokines such as interleukin 1β (IL-1β) and tumour necrosis factor alpha (TNF-α) increases. Taxifolin has been reported to suppress reactive oxygen species, IL-1β and TNF-α production. The aim of this study is to biochemically and histopathologically examine the protective effect of taxifolin against DR damage induced by alloxan. Alloxan received rats with a blood glucose level of ≥250 mg/dL were divided into taxifolin-treated (TAX) ( = 6), diabetic control (DC) ( = 6) groups. There were rats received only saline in non-diabetic control (NC) group ( = 6). Taxifolin (50 mg/kg) was orally administered to the TAX group rats. DC and NC rats received the same volume of saline as a solvent. This procedure was repeated once a day for 3 months. At the end of this period, animals were killed by high dose thiopental sodium anaesthesia. Histopathological examinations were then performed on excised rat eyes. Malondialdehyde (MDA), total glutathione (tGSH), IL-1β and TNF-α levels were measured in obtained blood samples. MDA, IL-1β and TNF-α levels were significantly increased in blood samples of DC group rats with hyperglycemia induced by alloxan compared with NC group ( < 0.0001), and decreased in the TAX group compared with the DC group ( < 0.0001). The levels of tGSH were significantly decreased in blood samples of DC group rats compared with NC group ( < 0.0001), and increased in the TAX group compared with the DC group ( < 0.0001). Histopathologically, retinal ganglion cells of the TAX group had a slightly dilated and congested blood vessel, and severe damage was inflicted to the retinal ganglion cell layer of the DC group. Experimental results suggest that taxifolin may be beneficial in the treatment of DR.