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Aryl piperazine suppresses cataractogenesis in a diabetic rat model via Nrf2/HO-1 signaling pathway
Abstract
Purpose: To investigate the inhibitory potential of aryl piperazine on cataract formation in diabetic rats, and the underlying mechanism of action.
Methods: Sprague-Dawley rats (7-week-old) were divided into 7 groups: control rats, untreated diabetic rats, and five aryl piperazine treatment groups given the drug at doses of 1, 2, 5, 10 and 15 mg/kg. Diabetes was induced in the rats via injection of streptozocin (STZ) in citrate buffer at a dose of 65 mg/kg. An ophthalmoscope was used to evaluate cataract formation, while GlucoLeader was used for the measurement of blood glucose level.
Results: Aryl piperazine treatment significantly reduced blood glucose level from 6 to 12 weeks following administration of STZ, and prevented cataractogenesis in the diabetic rats (p < 0.05). Cataract score in the diabetic rats was also significantly decreased by aryl piperazine (p < 0.01). Aryl piperazine exposure reversed STZ-mediated decreases in antioxidant capacity (AOC) and glutathione (GSH) levels, enhanced glutathione peroxidase (GPX) activity and decreased malondialdehyde (MDA) levels in diabetic rats (p < 0.05). It suppressed the expressions of vascular endothelial growth factor (VEGF) and interleukin (IL)-1β in retinal tissues, while it upregulated the expressions of nuclear factor erythroid 2- related factor 2 (NRF2) and heme oxygenase (HO-1).
Conclusion: Aryl piperazine suppresses cataractogenesis and reduces cataract score in diabetic rats by targeting oxidative stress. Moreover, in retinal tissues of diabetic rats, aryl piperazine activates Nrf2/mHO-1 signaling pathway. Thus, aryl piperazine has a potential for use in the prevention of cataracts.
