Combined vitamins C and E attenuate memory impairment and hippocampal damage in diabetic sleep-deprived mice: behavioral and molecular insights
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Published on: September 22, 2020
Fatemeh Habibnia1, Olia Hamzeh2, Manochehr Ashrafpour3
1Student Research Committee, Babol University of Medical Sciences, Babol, Iran, Islamic Republic of.
Background:
Diabetes mellitus (DM) and sleep disturbances are associated with cognitive impairment and hippocampal dysfunction, potentially involving oxidative stress and neuroinflammation.
Objective:
This study investigated the effects of vitamins C and E, individually and in combination, to determine whether their complementary antioxidant properties provide enhanced neuroprotective effects against cognitive and hippocampal alterations in diabetic sleep-deprived mice.
Methods:
Diabetes was induced in male BALB/c mice (25-30 g) by streptozotocin (60 mg/kg), followed by partial sleep deprivation using the inverted flowerpot method. Animals received vitamin C (50 mg/kg), vitamin E (100 mg/kg), or their combination for 20 days. Body weight and blood glucose were monitored. Spatial learning and memory were evaluated using the Morris water maze. Hippocampal histopathology, GFAP immunostaining, and expression of genes related to oxidative stress, inflammation, and neuroprotection were assessed.
Results:
Vitamin E and combined vitamin C and E treatment reduced FBG and were associated with higher final body weight than untreated diabetic sleep-deprived mice. Vitamin treatments improved spatial learning and memory, with combined treatment producing greater improvements in selected behavioral outcomes. Combined treatment increased hippocampal neuronal density and reduced GFAP immunoreactivity. Vitamin treatment increased BDNF, Nrf2, and HO-1 expression and reduced iNOS, TNF-α, and IL-1β expression.
Conclusion:
Vitamin C and E, particularly in combination, were associated with improved metabolic, cognitive, and hippocampal outcomes in diabetic sleep-deprived mice, potentially involving modulation of neuroinflammatory and oxidative stress-related markers.
