Neuroprotective effects of lycopene on lipopolysaccharide-induced cerebellar damage in rats: Implication for Alzheimer’s disease therapy

Abstract

BACKGROUND AND AIM: The alarming rise in Alzheimer's disease prevalence, projected to affect 153 million people by 2050, underscores the urgent need for effective treatments. Previous research implicates oxidative stress in the neuronal death mechanisms associated with Alzheimer's. Lycopene, a carotenoid, has demonstrated neuroprotective properties, reduced oxidative damage, and minimized histopathological changes in animal models of Alzheimer's disease. This study aimed to investigate the role of lycopene in lipopolysaccharide (LPS)-induced cerebellar toxicity in rats.

METHODS: Fifty adult Wistar rats were divided into five groups: A (control; non-pelletized rat feed, oil, and water), B treated with 150 mg/kg body weight of LPS only intraperitoneally, C treated with (LPS 150 mg/kg intraperitoneally + 15 mg/kg lycopene orally), D (15 mg/kg lycopene orally + 150 mg/kg LPS intraperitoneally), and E (15 mg/kg lycopene orally). The rats underwent neurobehavioral protocols, and post-sacrifice brain sections were processed and stained using H&E, Silver, and Luxol fast blue counter-stained with Nissl stain.

RESULTS: The LPS treatment group exhibited significant body weight loss and motor coordination impairments, indicated by increased orientation and transit times. Lycopene-treated groups showed mitigated weight loss and improved motor coordination. Histopathological analysis revealed mild neuronal damage in the LPS group, while lycopene-treated groups exhibited milder lesions.

CONCLUSION: Lycopene demonstrates significant neuroprotective effects in LPS-induced cerebellar damage in rats, improving motor coordination and reducing neuronal damage. These findings suggest lycopene's potential as a therapeutic agent for oxidative stress-related neurodegenerative conditions, such as Alzheimer's disease.