Neuroinflammation is a key component of the pathophysiology of neurodegenerative diseases. To date, the management of patients with neurodegenerative diseases is based on symptomatic treatments. In recent years, the scientific community has focused its research on the regulation of the neuroinflammation. In this thesis, we observed the potential anti-inflammatory and neuroprotective effects induced by an alpha 7 nicotinic acetylcholine receptor agonist (α7 nAChR), PHA 543613, in an in vivo neuroinflammatory model. These observations led us to continue our investigations through a mechanistic approach, and more precisely, to quantify the expression of a phase II antioxidant enzyme. By analogy with the peripheral anti-inflammatory cholinergic pathway, the activation of α7 nAChR localised on glial cells leads to the overexpression of heme oxygenase 1.