Effects of minocycline on acrylamide-induced neurotoxicity in Wistar rats.

Objectives: Acrylamide (ACR) causes neurotoxicity in animals and humans through oxidative stress, inflammation, and apoptosis. Male Wistar rats were used to evaluate the neuroprotective effects of minocycline on ACR-induced neurotoxicity. Materials and Methods: Animals were distributed into 11 groups: 1. Control (normal saline, 11 days, IP), 2. Normal saline (20 days), 3. ACR (50 mg/kg, 11 days, IP), 4. ACR (11 days, days 11-20 normal saline), 5, 6, 7. (Minocycline 10, 20, 40 mg/kg, IP+ ACR, 11 days) 8. (Minocycline 40 mg/kg, days 6-11), 9. Minocycline (40 mg/kg, days 6-20), 10. Minocycline (40 mg/kg, 11 days), 11. Vitamin E (200 mg/kg, every other day, IP) + ACR. The gait score was assessed at the end of the treatment period. Biochemical markers, including Malondialdehyde (MDA), glutathione (GSH), caspase-3, interleukin-1 beta (IL-1β), and tumor necrosis factor-α (TNF-α) were determined in the cerebral cortex. Results: Administration of ACR induced movement disorders, reduced GSH levels, and elevated MDA, TNF-α, IL-1β, and cleaved caspase-3 in the cerebral cortex. Co-administration of minocycline 40 mg/kg with ACR ameliorated gait score abnormality. Treatment with minocycline (40 mg/kg), initiated 6 days after ACR administration and continued for 20 days, attenuated movement disorders. Furthermore, intraperitoneal injection of minocycline (40 mg/kg) with ACR reduced the levels of MDA, IL-1β, and caspase-3-cleaved proteins in the cerebral cortex. Conclusion: Administration of minocycline exhibits both prophylactic and therapeutic properties against ACR-induced neurotoxicity primarily through anti-oxidant, anti-apoptotic, and anti-inflammatory properties.