小胶质细胞
HMGB1
神经保护
表型
巨噬细胞极化
促炎细胞因子
创伤性脑损伤
巨噬细胞
化学
细胞生物学
医学
免疫学
体外
药理学
生物
炎症
生物化学
基因
精神科
作者
Tielei Gao,Zhe Chen,He Chen,Hui Yuan,Yuena Wang,Peng Xue,Can Wei,Jing Yang,Chi Xu
标识
DOI:10.1016/j.bbrc.2018.02.102
摘要
Microglia/Macrophages have a double-edged role in secondary brain damage after traumatic brain injury (TBI) depending on polarization toward proinflammatory M1 or anti-inflammatory M2 phenotypes. Recently, high-mobility group box 1 (HMGB1) was found to influence the polarization of macrophages. In this study, glycyrrhizin (GL), an inhibitor of HMGB1, was used to investigate whether the inhibition of HMGB1 could modulate microglia/macrophage polarization after TBI. The results showed that treatment with GL improved the neurological function recovery, reduced the lesion volume, and inhibited the release and expression of HMGB1 after TBI. In addition, the administration of GL suppressed M1 phenotype activation and promoted M2 phenotype activation of microglia/macrophages. In conclusion, the results suggested that GL attenuated TBI by inhibiting M1 phenotype while inducing M2 phenotype activation of microglia/macrophages, at least partly through inhibiting HMGB1. Also, targeting HMGB1 to modulate the microglia/macrophage polarization should be one potential therapeutic approach for TBI.
科研通智能强力驱动
Strongly Powered by AbleSci AI