Neurological mechanism of the dietary supplementations of lycopene on chemotherapy-induced cognitive dysfunction/chemobrain and hippocampal toxicity in the rat model

Abstract

Chemo-brain signifies the memory and cognitive challenges cancer patients encounter during and after chemotherapy. Lycopene (LP) is a naturally occurring carotenoid with potent anti-reactive oxygen species (ROS) characteristics. This study investigates the effect of Lycopene on Chemotherapy-induced cognitive dysfunction and hippocampal toxicity in rat models. Thirty Adult male Sprague-Dawley rats were divided into five groups of five (n=6) rats each. Group A control received normal saline. Group B received a single dose of 10 mg/kg bwt cisplatin (CP, i.p.) on the first day. Group C received 100 mg/kg bwt of Lycopene (LP) (i.p) once daily. Group D received a single dose of 10 mg/kg CP (i.p.) on the first day, followed by 100 mg/kg bwt of LP (i.p) once daily. Group E was treated with 100 mg/kg bwt of LP (i.p) once daily, followed by a single dose of 10 mg/kg bwt CP (i.p.) on the last day. The experiment lasted for 28 days. Hippocampus histology, oxidative stress, neuro-inflammation, apoptotic markers, brain acetylcholinesterase (AChE) activity, and levels of dopamine (DA), gamma-aminobutyric acid GABA, and serotonin 5-HT were investigated. Lycopene attenuation of malondialdehyde and nitric oxide levels with elevated glutathione levels and intensified superoxide dismutase and catalase activities. Lycopene decreased the levels of inflammatory and apoptotic markers. In addition, LP reduced AChE activity, and elevated glial fibrillary acidic proteins increased neurotransmitter and brain-derived neurotrophic factors. Lycopene protected chemobrain rats, decreasing inflammation and apoptosis, increasing antioxidant enzyme activities, and attenuating lipid peroxidation.