Sinomenine enhances microglia M2 polarization and attenuates inflammatory injury in intracerebral hemorrhage.

Microglia polarization plays a vital role in brain inflammatory injury following intracerebral hemorrhage (ICH). Previous studies have shown that sinomenine possesses potential immunoregulatory capabilities. However, microglia polarization's exact mechanisms in ICH remain uncertain. Therefore, we examined the role of sinomenine on microglia polarization and brain inflammation following ICH. For the experiment, autologous blood models were constructed in C57/BL6 mice. Markers of classically activated (M1) and alternatively activated (M2) microglia were detected by real-time polymerase chain reaction, immunofluorescence, and flow cytometry. Microglial toxicity was assessed using MTT and FACS assays. In addition, the neurological deficit and cerebral water content of ICH mice were also observed. Sinomenine attenuated M1 markers while promoting M2 markers of microglia. Sinomenine also protected hippocampal neurons from indirect toxicity mediated by ICH-treated microglia. Additionally, administration of sinomenine inhibited matrix metalloproteinase (MMP) 3/9 expression, cerebral water content, and neurological deficit. Therefore, sinomenine protected brain function following ICH, perhaps via M2 microglia phenotype induction and MMP 3/9 inhibition. This result suggests that sinomenine is a promising therapeutical strategy in ICH.