The possible role of lycopene on the cerebellum of albino rat prenatally exposed to valproic acid: Animal model of autism spectrum disorder.

Autism is a serious neurodevelopmental disorder with a rising global prevalence. Prenatal exposure to valproic acid (VPA), a common antiepileptic drug, is associated with autism in offspring. Lycopene, a potent antioxidant and anti-inflammatory compound, may counteract VPA-induced neurotoxicity. To the best of our knowledge, this research is the first attempt to assess the beneficial role of lycopene supplementation in a VPA model of autism. In total, 30 pregnant female albino rats were grouped into five groups: control, lycopene-treated (5 mg/kg/day orally), VPA-treated (50 mg/kg/day orally), VPA-protected with lycopene, and VPA-treated with lycopene. After the scarification of rats, biochemical, histological, immunohistochemical, and ultrastructural analyses were performed on the cerebellum. VPA produced degenerative changes in the cerebellum with increased glial fibrillary acidic protein (GFAP) and Bax while decreasing myelin basic protein (MBP) and Tau1 expressions. Moreover, it increased the brain levels of malondialdehyde (MDA), acetylcholinesterase enzyme (AChE), tumor necrosis factor-alpha (TNF-α), and glutamate. It also reduced brain-derived neurotrophic factor (BDNF) and superoxide dismutase (SOD) levels. Lycopene reversed these effects by reducing oxidative stress and inflammatory markers, and restoring antioxidant levels. In conclusion, lycopene mitigated VPA-induced cerebellar damage through its antioxidant and anti-inflammatory effects and its ability to modulate neurotransmission, suggesting a potential therapeutic role in autism.