Hydroxychloroquine improves motor function and affords neuroprotection without inhibition of inflammation and autophagy in mice after intracerebral hemorrhage

We examined the effect of an immunomodulator hydroxychloroquine, also known as a Nurr1 ligand and an autophagy inhibitor, on a mouse model of intracerebral hemorrhage (ICH). Daily administration of hydroxychloroquine (100 mg/kg, i.p.) from 3 h after induction of ICH alleviated neurological deficits of mice, increased the number of surviving neurons in the hematoma and prevented fragmentation of axon structures in the internal capsule. Unexpectedly, hydroxychloroquine did not inhibit either upregulation of pro-inflammatory mediators or autophagic responses in the brain. Hence, hydroxychloroquine may produce therapeutic effects on ICH primarily via neuroprotection including preservation of the axon tract integrity. [Display omitted] •Hydroxychloroquine alleviated intracerebral hemorrhage (ICH)-induced motor deficits.•Hydroxychloroquine attenuated ICH-induced damage of neurons and axon tracts.•Hydroxychloroquine did not inhibit cytokine/chemokine expression after ICH.•Hydroxychloroquine did not inhibit autophagic responses in the brain after ICH.