Minocycline protects against lipopolysaccharide-induced glial cells activation and oxidative stress damage in the medial prefrontal cortex (mPFC) of the rat

Purpose/Aim Neuroinflammation and oxidative stress have been encountered in neurodegenerative diseases such as Alzheimer's disease (AD). However, the neuroprotective effects of minocycline against lipopolysaccharide (LPS)-induced glial cells activation and oxidative stress damage in the medial prefrontal cortex (mPFC) of rats are still elusive. The purpose of this study is to investigate the effects of minocycline and memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist, on the microglia and astrocytes expression, as well as oxidative stress levels in the mPFC of LPS injected rats. Materials and Methods Fifty adult Male Sprague Dawley rats were divided into five groups: control, LPS (5 mg/kg), LPS treated with minocycline (25 mg/kg), LPS treated with minocycline (50 mg/kg) and LPS treated with memantine (10 mg/kg). The immunohistochemistry and western blotting were used to analyse the expressions and densities of microglia marker (Iba-1) and astrocyte marker, (GFAP) while enzyme-linked immunosorbent assay (ELISA) was used to measure the protein carbonyl (PCO), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels. Results In comparison to the control group, the expression and density of Iba-1 and GFAP were significantly enhanced in the LPS group (p < 0.05). LPS group also exhibited significantly higher levels of PCO and MDA (p < 0.05) and significantly lower levels of CAT and SOD (p < 0.05) when compared to the control group. Both minocycline and memantine-treated LPS rats were able to protect against these effects. Conclusion Minocycline, like memantine treatment, reduces oxidative stress in the mPFC of LPS rats via inhibition of glial cells activation.