1. Prophylactic effects of apigenin against hyperglycemia-associated amnesia via activation of the Nrf2/ARE pathway in zebrafish.
- Author
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Haridevamuthu B, Ranjan Nayak SPR, Murugan R, Pachaiappan R, Ayub R, Aljawdah HM, Arokiyaraj S, Guru A, and Arockiaraj J
- Subjects
- Animals, Acetylcholinesterase metabolism, Signal Transduction drug effects, Brain drug effects, Brain metabolism, Brain pathology, Antioxidants pharmacology, Antioxidants therapeutic use, Zebrafish Proteins metabolism, Blood Glucose metabolism, Blood Glucose drug effects, Male, Streptozocin, Maze Learning drug effects, Spatial Memory drug effects, Disease Models, Animal, Zebrafish, NF-E2-Related Factor 2 metabolism, Hyperglycemia complications, Hyperglycemia drug therapy, Hyperglycemia metabolism, Amnesia drug therapy, Amnesia metabolism, Oxidative Stress drug effects, Apigenin pharmacology, Apigenin therapeutic use, Neuroprotective Agents pharmacology, Neuroprotective Agents therapeutic use
- Abstract
The escalating focus on ageing-associated disease has generated substantial interest in the phenomenon of cognitive impairment linked to diabetes. Hyperglycemia exacerbates oxidative stress, contributes to β-amyloid accumulation, disrupts mitochondrial function, and impairs cognitive function. Existing therapies have certain limitations, and apigenin (AG), a natural plant flavonoid, has piqued interest due to its antioxidant, anti-inflammatory, and anti-hyperglycemic properties. So, we anticipate that AG might be a preventive medicine for hyperglycemia-associated amnesia. To test our hypothesis, naïve zebrafish were trained to acquire memory and pretreated with AG. Streptozotocin (STZ) was administered to mimic hyperglycemia-induced memory dysfunction. Spatial memory was assessed by T-maze and object recognition through visual stimuli. Acetylcholinesterase (AChE) activity, antioxidant enzyme status, and neuroinflammatory genes were measured, and histopathology was performed in the brain to elucidate the neuroprotective mechanism. AG exhibits a prophylactic effect and improves spatial learning and discriminative memory of STZ-induced amnesia in zebrafish under hyperglycemic conditions. AG also reduces blood glucose levels, brain oxidative stress, and AChE activity, enhancing cholinergic neurotransmission. AG prevented neuronal damage by regulating brain antioxidant response elements (ARE), collectively contributing to neuroprotective properties. AG demonstrates a promising effect in alleviating memory dysfunction and mitigating pathological changes via activation of the Nrf2/ARE mechanism. These findings underscore the therapeutic potential of AG in addressing memory dysfunction and neurodegenerative changes associated with hyperglycemia., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)
- Published
- 2024
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