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Intracerebral hemorrhage (ICH) is a devastating stroke subtype. Baicalein (BAI) has been reported to be effective in ischemic stroke. The aim of the present study was to investigate the mechanism of BAI on brain injury after ICH. Firstly, ICH mouse models were established by injecting collagenase into the right of basal ganglia, followed by detection of neurobehavioral scores, brain edema, oxidative stress (OS) level, neuronal apoptosis and pathological changes. Average neurologic scores, brain water content, and blood–brain barrier permeability and MDA level in ICH mice were reduced after BAI treatment, while serum SOD and GSH-Px levels were increased and neuronal apoptosis and pathological injury of the brain tissues were mitigated. miR-106a-5p downregulation averted the effect of BAI on ICH mice. miR-106a-5p targeted PHLPP2 and PHLPP2 overexpression reversed the effect of BAI on ICH mice. BAI activated the Nrf2/ARE pathway by inhibiting PHLPP2 expression. In conclusion, BAI inhibited OS and protected against brain injury after ICH by activating the Nrf2/ARE pathway through the miR-106a-5p/PHLPP2 axis.

Baicalein ameliorates oxidative stress and brain injury after intracerebral hemorrhage by activating the Nrf2/ARE pathway via miR-106a-5p/PHLPP2 axis