Bromelain Administration Ameliorates Neurobehavioural Deficits Mediated by Cadmium Neurotoxicity via Oxido-Nitrosative Stress, Cholinergic and Neuroinflammatory Modulations in Male Wistar Rats

Abstract

Cadmium (Cd) is a toxic metal widely present in the environment. Certain plant-based natural or active compounds are gaining attention for their neuroprotective effects against chemically induced toxicity. However, there is no report on the impact of bromelain on Cd-induced neurotoxicity, hence the rationale behind this study. Twenty-four adult male rats were divided into four groups: control (normal saline, 5mL/kg), Cd (orally, 5mg/kg), bromelain (50mg/kg), and Cd+bromelain. Rats received bromelain or normal saline for 14 days. Cd was administered concurrently with bromelain and normal saline in the last 7 days. Neurobehavioural responses to locomotion, cognition, anxiety, and depression were assessed. Plasma was assayed for the levels of superoxide dismutase (SOD) and malondialdehyde (MDA), while the prefrontal cortex (PFC) was processed for the concentration of Cd and levels of SOD, MDA, nitric oxide (NO), acetylcholinesterase (AChE), interleukin-6 (IL-6), and tumour necrotic factor-α (TNF-α). Data were analysed using one-way ANOVA (Tukey’s post hoc), with the level of significance set at p<0.05. Exposure to Cd caused a significant behavioural deficit, as indicated by a decline in motor coordination, memory index, and enhanced depressive and anxiety-like behaviours. Biochemically, Cd concentration was significantly increased in the PFC of Cd group compared to the control. There was a reduction in the level of SOD and increased levels of MDA, NO, IL-6, AChE, and TNF-α following Cd exposure. Bromelain significantly improved the behavioural outcomes and reversed some of the biochemical markers altered by Cd toxicity. Bromelain reduced neurobehavioural impairment, cholinergic alteration, and oxido-inflammatory deficits induced by Cd exposure.