Effects of M2 Polarization of Microglia on Inflammatory Injury in Cerebral Hemorrhage
Department of Neurosurgery, Tongde Hospital of Zhejiang Province, No.234 Gucui Road, Hangzhou 310012, China
Department of Neurosurgery, Tongde Hospital of Zhejiang Province, No.234 Gucui Road, Hangzhou 310012, China, E-mail: email@example.com
In this study, C57BL/6 mice were used to construct an animal model of cerebral hemorrhage to investigate the effect of M2 polarization of microglia on inflammation injury of cerebral hemorrhage. Regulatory T cells were sorted by immunomagnetic beads, while Western Blot was used to detect the expression of phosphorylation signal transduction and transcription activator 3, T-signal transduction and transcription activator 3, transforming growth factor-β and β-actin in each group. Enzyme linked immunosorbent assay was used to detect the level of specific antibodies to explore the correlation between M2 polarization of microglia and inflammation injury. Results showed that the expression of an M2 microglia marker chitinase 3-like 3 and M1-related cytokines, interleukin-6 and tumor necrosis factor α were increased significantly in the regulatory T cell -treated group, along with significantly decreased expressions of an M1 marker and M2-related cytokines, interleukin-10 and transforming growth factor-β. It was hypothesized that regulatory T cells could regulate M2 polarization of microglia through interleukin-10/signal transduction and transcription activator 3 signaling pathway. In addition, the expression of M2 microglia markers Arg1 and Ym1 increased in the regulatory T cell-treated group, along with decreased expressions of M1 microglia markers, chemokine (C-C motif) ligand 3 and inducible nitric oxide synthase. It was also confirmed that regulatory T cells could induce the M2 polarization of microglia.