Lens-protective Effects of Hesperidin and Naringenin in a Rat Model of Streptozotocin-Induced Diabetes Mellitus

Diabetic cataract is driven by hyperglycemia-associated oxidative/nitrosative stress, inflammation, apoptosis, activation of the polyol pathway, and lens protein glycation. Hesperidin (HSN) and Naringenin (NGN) are citrus flavonoids with antioxidant, anti-inflammatory, anti-apoptotic, and antidiabetic activities. This study evaluated their lens-protective effects in streptozotocin (STZ)-induced diabetic rats.

Male Sprague-Dawley rats with STZ-induced diabetes received hesperidin (100 mg/kg/day, orally) or naringenin (50 mg/kg/day, orally) for 10 weeks. Fasting blood sugar, serum insulin, lenticular malondialdehyde, nitric oxide, total antioxidant capacity, TNF-alpha, IL-6, NF-kB p65, Bax/Bcl-2 ratio, cleaved caspase-3, aldose reductase activity, sorbitol concentration, glycated proteins, and total/soluble proteins were assessed.

STZ significantly increased fasting blood sugar and reduced serum insulin. Diabetic lenses also showed increased levels of malondialdehyde, nitric oxide, TNF-alpha, IL-6, NF-kB p65, Bax/Bcl-2 ratio, cleaved caspase-3, aldose reductase activity, sorbitol, and glycated proteins, with reduced total antioxidant capacity and total/soluble protein levels. HSN and NGN significantly ameliorated these changes versus untreated diabetic rats (p < 0.05).

The findings indicate that HSN and NGN mitigate biochemical pathways implicated in diabetic lens injury, including oxidative/nitrosative stress, inflammation, apoptosis, polyol-pathway activation, and protein glycation.

In this STZ-induced rat model, hesperidin and naringenin preserved lens biochemical homeostasis and attenuated diabetes-associated lens injury, supporting their potential as adjunctive candidates for preventing or delaying diabetic lens damage.