Abstract
Traumatic brain injury (TBI) poses a significant risk to neurological function, primarily attributable to oxidative stress. Our hypothesis suggests that honey, renowned for its high phenol and flavonoid content, exerts neuroprotective effects by mitigating oxidative stress. This study aims to assess honey's potential as an innovative therapeutic agent in a TBI rat model, primarily focusing on its impact on behaviour, lipid peroxidation, and antioxidant enzyme activity. A total of twenty adult male Wistar rats were randomly divided into four groups: Group A (control), Group B (honey-treated), Group C (TBI-induced), and Group D (honey-treated TBI). We conducted comprehensive assessments using the Rotarod and Elevated Plus Maze tests to evaluate behaviour. Additionally, biochemical evaluations included quantifying lipid peroxidation levels and conducting a detailed analysis of antioxidant enzyme status, specifically emphasising the activity of glutathione (GSH) and catalase (CAT). Our findings indicated that the TBI model rats displayed impaired motor coordination, heightened anxiety-like behaviour, and elevated lipid peroxidation levels. Intriguingly, the honey treatment effectively reversed these behavioural deficits while concurrently reducing lipid peroxidation. Notably, honey treatment significantly augmented the activity of antioxidant enzymes (CAT and GSH); there was a significant increase in CAT activity compared to GSH activity in the treated TBI model. This study supports our hypothesis, demonstrating that honey is a potent neuroprotective agent that counteracts TBI-induced oxidative stress. Our investigation elucidates honey's capacity to alleviate neurobehavioral impairments and mitigate oxidative damage within a TBI model. These results underscore honey's significance as an innovative and promising therapeutic approach in TBI management, emphasizing its potential to enhance neurological outcomes and improve the overall well-being of individuals affected by TBI.
Published Version
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