Effects of minocycline on acrylamide-induced neurotoxicity in Wistar rats

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.

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.

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.

Administration of minocycline exhibits both prophylactic and therapeutic properties against ACR-induced neurotoxicity primarily through anti-oxidant, anti-apoptotic, and anti-inflammatory properties.