Methyl jasmonate inhibits MPP+-induced neuroinflammation and oxidation in BV2 microglia cells Via NF-kB (p65)/Nrf2 pathway

Parkinson's disease (PD) is the most common neurodegenerative movement disorder characterized by neuroinflammation, oxidation and apoptosis. Compounds and mechanisms that regulate these hallmarks are great targets for PD therapy. Methyl Jasmonate (MJ) has been conferred with anti-inflammatory, antioxidative, and anti-apoptotic properties, but its role in BV-2 models of PD is unknown. This study investigated the neuroprotective role of methyl jasmonate on BV-2 microglia cells stimulated with 1-methyl-4-phenylpyridinium (MPP+) neurotoxin. The objectives of the study were to: (i) investigate the neuroprotective effects of MJ on (MPP+)-induced neurotoxicity in BV-2 microglia cells; and (ii) determine the mechanisms by which MJ exerts these neuroprotective effects. BV-2 microglia cells were pre-treated with MJ for 30 minutes and stimulated with MPP+ for 24 hours. The treatment groups are: (A) control (dimethyl sulfoxide); (B) MPP+ (100μM); (C) MJ (5μM) plus MPP+ (100μM); (D) MJ (10μM) plus MPP+ (100μM); (E) MJ (20μM) plus MPP+ (100μM); and (F) MJ (40μM) plus MPP+ (100μM). Cell viability, pro-inflammatory cytokines, and enzymes levels were assayed. Levels of iNOS, cyclooxigenase-2, DNA binding and Nrf2 were also determined. One-way analysis of variance and post hoc Tukey's test were used for statistical analysis at p < 0.05. The findings of the study showed that MJ significantly (p < 0.05): (i) inhibited MPP+-induced neurotoxicity and promoted the viability of BV2 microglia cells; (ii) reduced MPP+-induced production of cytokines; (iii) suppressed MPP+-induced expression of pro-inflammatory enzymes when compared with MPP+ only group; (iv) inhibited MPP+-induced neuroinflammation via NF-kB inactivation and suppressed MPP+-induced nuclear accumulation of NF-kB when compared with MPP+ only group; (v) suppressed MPP+-induced expression of Nrf2 when compared with MPP+ only group. This study concluded that methyl jasmonate protected BV-2 microglia cells against (MPP+)-induced neuroinflammation and oxidation via NF-kB(p65)/Nrf2 pathway.