Exploration of neuroprotective effect of vanillin on Cobalt induced neurotoxicity in rat model

Abstract

Background: Cobalt chloride (CoCl₂) induces neurotoxicity by stabilizing hypoxia-inducible factor-1 alpha (HIF-1α), leading to oxidative stress, neuroinflammation, mitochondrial dysfunction, and cognitive impairment. Vanillin (4-hydroxy-3-methoxybenzaldehyde), a naturally occurring phenolic aldehyde isolated from Vanilla planifolia, possesses antioxidant, anti-inflammatory, anti-apoptotic, and neuroprotective properties (Arya et al., 2021; Iannuzzi et al., 2023). Objective: To investigate the neuroprotective potential of vanillin against CoCl₂-induced neurotoxicity in Sprague Dawley rats. Material and Methods: Male Sprague Dawley rats (170–200 g; n=6/group) were divided into four groups: normal control, negative control (CoCl₂ 40 mg/kg/day p.o. for 14 days), CoCl₂ + vanillin 100 mg/kg/day, and CoCl₂ + vanillin 200 mg/kg/day. Behavioral assessments included Morris Water Maze (MWM), Elevated Plus Maze (EPM) Results: CoCl₂ significantly increased escape latency (71 ± 1.2 s; p < 0.01) and reduced retention time (13 ± 1.4 s; p < 0.01) in the MWM, and elevated transfer latency (68.9 ± 3.4 s; p < 0.01) in the EPM, confirming impaired spatial memory and anxiety-like behaviour. Vanillin treatment dose-dependently reversed these deficits; the 200 mg/kg dose maximally restored escape latency (27 ± 0.75 s), retention time (30 ± 1.4 s), and transfer latency (27.8 ± 1.8 s) compared to the negative control (all p < 0.01). Conclusion: Vanillin demonstrated significant dose-dependent neuroprotective effects against CoCl₂-induced neurotoxicity through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. These findings support the potential therapeutic role of vanillin in oxidative stress-mediated neurodegenerative disorders.