A Nurr1 agonist amodiaquine attenuates inflammatory events and neurological deficits in a mouse model of intracerebral hemorrhage.

Inflammatory responses are considered to play pivotal roles in the pathogenesis of intracerebral hemorrhage (ICH). Here we show that a nuclear receptor Nurr1 (NR4A2) was expressed prominently in microglia/macrophages and astrocytes in the perihematomal region in the striatum of mice after ICH. Daily administration of a Nurr1 agonist amodiaquine (40 mg/kg, i.p.) from 3 h after ICH induction diminished perihematomal activation of microglia/macrophages and astrocytes. Amodiaquine also suppressed ICH-induced mRNA expression of IL-1β, CCL2 and CXCL2, and ameliorated motor dysfunction of mice. These results suggest that Nurr1 serves a novel target for ICH therapy.