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Updated: Jan 9, 2026
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
KLF2-mediated activation of Nrf2-HO-1 pathway modulates microglia/macrophage polarization post-ischemic stroke
Gui-Yuan Huang1, Hong-Miao Tao1, Yuan-Yuan Wu1
1Medical College, Jinhua University of Vocational Technology, Jinhua, China.
Background:
Shifting the microglia/macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype shows promise in developing therapeutic strategies after ischemic stroke (IS). The study is aimed to investigate the role of krueppel-like factor 2 (KLF2) in modulating microglia/macrophage polarization during IS.
Methods:
Mice received a 60-min middle cerebral artery occlusion (MCAO) and BV-2 cells underwent oxygen-glucose deprivation/reperfusion (OGD/R) treatment to induce IS-like injury in vivo and in vitro.
Results:
The mice subjected to MCAO exhibited impaired neurobehavioral performance, lower expressions of KLF2, Nrf2 and HO-1 in the peri-infarct cortex than the sham operated mice. Lentivirus-mediated KLF2 overexpression could effectively reduce the size of brain infarct, improve the recovery of neurobehavioral functions, and activate the Nrf2-HO-1 pathway in the mice subjected to MCAO. In addition, KLF2 overexpression led to M1 suppression and increase in M2 phenotype in OGD/R-insulted BV-2 microglial cells. Nrf2 knockdown was found to impair the effects of KLF2 overexpression on status of M1 and M2 phenotypes in OGD/R-insulted BV-2 cells.
Conclusion:
The study unveils KLF2 is neuroprotection and could promote microglia/macrophage polarization from the M1 to M2 phenotype in IS by activating the Nrf2-HO-1 pathway.
