Hesperidin induced attenuation of oxidative damage and restoration of antioxidant potential in induced diabetic neuropathy model of mice

Abstract

Oxidative stress is a major contributor to diabetes-associated neural injury, in which excessive
reactive oxygen species (ROS) promote lipid peroxidation, protein oxidation and depletion of cellular
reducing capacity. Hesperidin, a citrus-derived flavanone glycoside, has attracted considerable interest
because of its antioxidant and neuroprotective properties. The present study investigated the effects of
hesperidin on lipid peroxidation, oxidative protein modification, and ferric-reducing antioxidant capacity in
the brain of alloxan-induced diabetic mice. Diabetes was induced by a single administration of alloxan (170
mg/kg b.w.). Alloxan-induced diabetes produced a pronounced oxidative imbalance in brain tissue. Compared
with Group I, thiobarbituric acid reactive substances (TBARS) and protein carbonyl content (PCC) levels in
Group II increased by 170.59% and 66.19%, respectively, indicating increased lipid peroxidation and
oxidative protein modification. Hesperidin treatment in Group VI attenuated these alterations, with TBARS
and PCC levels decreasing by 17.66% and 13.83%, respectively, relative to Group II. In addition, ferric
reducing antioxidant power (FRAP) was 87.35% higher in Group VI than in Group II, indicating an
enhancement of the ferric-reducing capacity of brain tissue following hesperidin treatment. Overall, hesperidin
attenuated lipid and protein oxidative damage and enhanced reducing antioxidant capacity under diabetic
conditions. These findings provide biochemical evidence supporting the potential protective role of hesperidin
against diabetes-associated cerebral oxidative injury in experimental diabetic neuropathy (DN).