Parkinson’s disease (PD) is a neurodegenerative disorder characterized by tremors, spasms, involuntary movements and the loss of dopaminergic neurons. The degeneration of dopamine neurons during PD is concurrent with the release of pro-inflammatory cytokines that cause inflammation in the brain. This can reduce the neuroprotective effects of the microglia, by inhibiting their phagocytic response. With this in mind, we investigated the ability of nicotine and ibuprofen (a non-steroidal anti-inflammatory drug) to stimulate the release of anti-inflammatory cytokines and stabilize the phagocytic activity of microglia in an inflamed environment. Nicotine has long been thought to be a carcinogen found in tobacco cigarettes and more recently E-cigarettes. Although public consensus shows a negative reception, recent in vivo and in vitro studies have supported the use of low doses of nicotine as a potentially anti-inflammatory compound. Epidemiological studies suggest that smokers tend to have a lower incidence of PD. BV-2 microglial cells were first treated with nicotine or ibuprofen at concentrations 1 µM, 10 µM and 100 µM. Following a 24-hour incubation period, cells were then treated with an α-synuclein peptide and left to incubate for another 24 hours. Phagocytic activity was measured using fluorescently-tagged E. coli particles and quantified using ImageJ. Our experiments found that specific doses of nicotine and ibuprofen stabilized phagocytic activity in microglia incubated in neurotoxic environments induced by α-synuclein. These data support the utility of anti-inflammatory compounds in the regulation of phagocytosis in microglia and their potential as a mechanism for therapeutic treatments of PD
