Abstract
Diabetes, characterized by elevated blood glucose levels and associated organ damage, is reportedly correlated with adecline in cognitive functions with a potential involvement of oxidative stress mechanisms. Mitochondria-induced oxidative stress reported to cause hyperglycemia is believed to impair hippocampal neural plasticity, affecting long-term potentiation, and isconsidered crucial for maintaining memory functions. In this study, the neuroprotective effect of Pentoxifylline (PTX) for four weeks, an agent known for antioxidant and anti-inflammatory properties, was examined in an animal model of diabetes. In a streptozotocin (STZ) diabetic model, rats received intraperitoneal PTX (100 mg/kg), and learning and memory functions were tested using the radial arm water maze. STZ-treated diabetic rats exhibited impaired learning and memory functions (short/long-term, P < 0.05), whereas PTX treatment prevented these deficits. PTX treatment normalized diabetes-induced reduction in the protein expression levels of two enzymes of antioxidant defense superoxide dismutase and glutathione peroxidase (P < 0.05) in the hippocampal brain tissues. PTX treatment also mitigated STZ-induced increase in lipid peroxidation (TBARS, P < 0.05). Furthermore, reduced/oxidized glutathione (GSH/GSSG) ratios were enhanced in PTX-treated diabetic rats (P < 0.05), emphasizing the importance of redox balance restoration. However, PTX treatment did not significantly affect theantioxidant defense enzyme catalase activity. In conclusion, STZ-induced diabetes resulted in learning and memory impairment in rats, while PTX treatment prevented these effects, most likely via enhancement of antioxidant defense in the brain. This study highlights PTX’s potential neuroprotective benefits, providing translational insights into the issue of diabetes-related cognitive complications.
Published Version
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