Effects of minocycline on acrylamide-induced neurotoxicity in Wistar rats

Objective(s): 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 ۱۱ groups: ۱. Control (normal saline, ۱۱ days, IP), ۲. Normal saline (۲۰ days), ۳. ACR (۵۰ mg/kg, ۱۱ days, IP), ۴. ACR (۱۱ days, days ۱۱-۲۰ normal saline), ۵, ۶, ۷. (Minocycline ۱۰, ۲۰, ۴۰ mg/kg, IP+ ACR, ۱۱ days) ۸. (Minocycline ۴۰ mg/kg, days ۶-۱۱), ۹. Minocycline (۴۰ mg/kg, days ۶-۲۰), ۱۰. Minocycline (۴۰ mg/kg, ۱۱ days), ۱۱. Vitamin E (۲۰۰ 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-۳, interleukin-۱ beta (IL-۱β), 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-۱β, and cleaved caspase-۳ in the cerebral cortex. Co-administration of minocycline ۴۰ mg/kg with ACR ameliorated gait score abnormality. Treatment with minocycline (۴۰ mg/kg), initiated ۶ days after ACR administration and continued for ۲۰ days, attenuated movement disorders. Furthermore, intraperitoneal injection of minocycline (۴۰ mg/kg) with ACR reduced the levels of MDA, IL-۱β, and caspase-۳-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.

کلیدواژه ها:

Anti-oxidant ، Apoptosis ، Minocycline ، Neurotoxicity ، Oxidative stress