Eupatilin inhibits microglia activation and attenuates brain injury in intracerebral hemorrhage.

Inflammation serves a critical role in the pathophysiology of intracerebral hemorrhage (ICH)-induced brain injury. Eupatilin, a pharmacologically active flavone derived from Artemisia sp., has been reported to have antioxidant, anti-inflammatory, anti-allergic and antitumor activities. However, the effect of eupatilin in ICH has not been well studied. The aim of the present study was to investigate the effect of eupatilin on ICH-induced microglial inflammation. The MTT and Transwell migration assay results revealed that eupatilin significantly inhibited microglial migration. It also decreased the production of inflammatory cytokines in erythrocyte lysis-induced BV2 cells, as well as the level of intracellular reactive oxygen species. The anti-inflammatory mechanism of eupatilin was also investigated using ELISAs and western blotting and the results demonstrated that eupatilin was able to inhibit erythrocyte lysis-induced NF-κB activation in BV2 cells. Taken together, the results of the present study suggest that eupatilin serves neurological protective effects via inhibiting microglial inflammation, providing an experimental basis for the use of eupatilin as a therapeutic target for ICH.