Histological study of Astaxanthin’s neuroprotective potential in alleviating cisplatin-induced cerebellar cortex damage in adult male rats

Cisplatin (CIS) is a widely used chemotherapeutic agent with proven efficacy against various malignancies; however, its clinical utility is often constrained by dose-dependent neurotoxicity. This study investigated the histopathological, ultrastructural, and biochemical effects of astaxanthin (AST), a potent antioxidant, on the cerebellar cortex in a rat model of CIS-induced neurotoxicity. Twenty-four adult male Sprague Dawley rats were randomly assigned to four groups: Control, AST, CIS, and AST + CIS. CIS was administered intraperitoneally (10 mg/kg), while AST was given orally (20 mg/kg) for 10 consecutive days. CIS administration induced marked alterations in the cerebellar cortex, including Purkinje cell shrinkage, dendritic loss, and neuronal vacuolation, accompanied by reduced glutathione (GSH) and elevated malondialdehyde (MDA) levels, indicating oxidative stress. Co-treatment of CIS with AST significantly ameliorated these changes, preserving cerebellar architecture, Purkinje cell morphology, and restoring antioxidant balance. These findings suggest that AST exerts neuroprotection against CIS-induced cerebellar toxicity, likely through its antioxidant and anti-apoptotic properties. Further studies are warranted to clarify the underlying molecular pathways and evaluate AST potential as an adjuvant in CIS-based chemotherapy.