Table of Contents Author Guidelines Submit a Manuscript
Neural Plasticity
Volume 2017 (2017), Article ID 5405104, 11 pages
Review Article

The Polarization States of Microglia in TBI: A New Paradigm for Pharmacological Intervention

1Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Jiefang Road 88th, Hangzhou 310016, China
2Department of Neurosurgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Road 3rd, Hangzhou 310016, China

Correspondence should be addressed to Gao Chen

Received 28 October 2016; Revised 17 December 2016; Accepted 11 January 2017; Published 1 February 2017

Academic Editor: Mario Zuccarello

Copyright © 2017 Hangzhe Xu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Traumatic brain injury (TBI) is a serious medical and social problem worldwide. Because of the complex pathophysiological mechanisms of TBI, effective pharmacotherapy is still lacking. The microglial cells are resident tissue macrophages located in the brain and have two major polarization states, M1 phenotype and M2 phenotype, when activated. The M1 phenotype is related to the release of proinflammatory cytokines and secondary brain injury, while the M2 phenotype has been proved to be responsible for the release of anti-inflammation cytokines and for central nervous system (CNS) repair. In animal models, pharmacological strategies inhibiting the M1 phenotype and promoting the M2 phenotype of microglial cells could alleviate cerebral damage and improve neurological function recovery after TBI. In this review, we aimed to summarize the current knowledge about the pathological significance of microglial M1/M2 polarization in the pathophysiology of TBI. In addition, we reviewed several drugs that have provided neuroprotective effects against brain injury following TBI by altering the polarization states of the microglia. We emphasized that future investigation of the regulation mechanisms of microglial M1/M2 polarization in TBI is anticipated, which could contribute to the development of new targets of pharmacological intervention in TBI.