Bromelain Restores Glutamatergic Homeostasis via Regulation of NR2A, GLT-1, EAAC1, and xCT in Arsenic-Induced Cerebral Cortex and Hippocampal Neurotoxicity

Hippocampal-dependent cognitive impairment induced by chronic exposure to arsenic occurs through excitotoxicity. Pineapple proteolytic enzyme bromelain exhibits neuroprotective effects; however, its role in modulating glutamate-mediated toxicity remains unclear. This study examined the action of bromelain in arsenic-induced cognitive impairment based on the regulation of the NMDA receptor and glutamate transporter in the prefrontal cortex and hippocampus of rats. Seventy-two male Wistar rats were randomized into nine groups (n=8): control; arsenic-only (20 mg/kg, 14 days); three bromelain-only groups (5, 10, 15 mg/kg); three arsenics + bromelain groups (same arsenic dose plus bromelain for 14 days); and arsenic + donepezil (2 mg/kg). Behavioral evaluation was carried out using the Morris water maze, whereas ELISA and RT-qPCR were used to assess brain glutamate levels and gene expression of NR2A, xCT, EAAC1, and GLT1. Below are raw data for •Escape Latency •Mean Glutamate Levels (mM)•NR2A (PFC & HPC)•xCT (PFC & HPC)•EAAC1 (PFC & HPC)•GLT1 (PFC & HPC)