Intracerebral haemorrhage (ICH) is a common and devastating cerebrovascular disease with high morbidity and mortality, and its pathophysiological mechanisms were complex and still unclear. Increasing researches reported that microRNAs (miRNAs) played an important role in ICH-induced brain injury and microglial activation. In this study, we investigated the biological function of miR-590-5p and explored its molecular mechanism in ICH mice. The results of qRT-PCR showed that miR-590-5p expression level was down-regulated in perihematomal brain samples of ICH mice compared with that of sham group. In LPS-induced microglia cells, miR-590-5p level was also down-regulated at 24 h post-LPS compared with that of control group. Moreover, miR-590-5p overexpression remarkably increased the cerebral water content and neurological severity scores compared with that of scramble group in ICH mice. The production of inflammatory cytokine including IL-6, interleukin (IL)-1 beta, and tumor necrosis factor (TNF)-alpha in ICH mice was notably inhibited by miR-590-5p overexpression. Furthermore, the results of dual-luciferase reporter assay indicated that Pellino-1 (Peli1) was a direct target of miR-590-5p. MiR-590-5p overexpression remarkably inhibited the Peli1 gene expression both mRNA and protein levels. In addition, Peli1 overexpression partly abrogated the inhibitory effect of miR590-5p mimic. Taken together, these datas suggested that miR-590-5p attenuated brain injury in ICH mice through inhibiting Peli1 gene expression, indicating that miR-590-5p may be a promising molecular target for ICH treatment. (C) 2018 Elsevier Inc. All rights reserved.