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Updated: Oct 17, 2025
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
Translocator Protein Regulate Polarization Phenotype Transformation of Microglia after Cerebral Ischemia-reperfusion
Shadamu Yusuying1, Shalayiding Yusuyin2, Xiaojiang Cheng3
1Department of Neurosurgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, Xinjiang Uygur Autonomous Region, China; The First School of Clinical Medicine, Xinjiang Medical University, Urumqi 830011, Xinjiang Uygur Autonomous Region, China.
Abstract:
Microglia cells are activated after cerebral ischemia-reperfusion injury (CIRI), playing a dual role in aggravating the injury or promoting tissue repair by polarization. Translocator protein (TSPO) is a biomarker of neuroinflammation or microglia activation. Its expression is significantly increased while brain injury and neuroinflammation occur. However, the relationship between TSPO and microglia polarization in CIRI is still not clear. In the present study, the middle cerebral artery occlusion (MCAO) methods in rats were used to simulate CIRI. We found that the expressions of M1 markers (CD86, IL-1β, and TNF-α) and M2 markers (CD206, IL-10, and TGF-β) were significantly increased. Moreover, the injection of TSPO ligand, PK11195, inhibited the increase of M1 polarization markers but promoted the expressions of M2 polarization markers, which significantly ameliorated the neurological damage after MCAO in rats. In vitro studies showed that shRNA-mediated TSPO knock-down promoted M1 polarization but inhibited M2 polarization, accompanied by a significant decrease in cell viability. On the contrary, overexpression of TSPO inhibited M1 polarization, promoted M2 polarization, and significantly improved cell viability. In summary, TSPO plays a neuroprotective role in CIRI by inhibiting M1 polarization and promoting M2 polarization, which suggests that TSPO may have the potential to serve as a therapeutic target for stroke.
Insights
Translocator protein (TSPO) shows neuroprotective effects in cerebral ischemia-reperfusion injury (CIRI). Targeting TSPO may offer a novel therapeutic strategy for stroke by modulating microglia polarization.
Area of Science:
- Neuroscience
- Immunology
Background:
- Microglia activation and polarization are critical in cerebral ischemia-reperfusion injury (CIRI).
- Translocator protein (TSPO) is a marker for neuroinflammation and microglia activation, but its role in microglia polarization during CIRI is unclear.
Purpose of the Study:
- To investigate the role of TSPO in microglia polarization following cerebral ischemia-reperfusion injury (CIRI).
- To explore the therapeutic potential of targeting TSPO for stroke treatment.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in rats to simulate CIRI.
- In vivo and in vitro studies assessing microglia polarization markers (M1 and M2) and cell viability.
- Administration of TSPO ligand (PK11195) and TSPO knockdown/overexpression via shRNA.
Main Results:
- TSPO ligand PK11195 inhibited M1 polarization markers and promoted M2 markers, reducing neurological damage in MCAO rats.
- TSPO knockdown in vitro promoted M1 polarization and decreased cell viability.
- TSPO overexpression in vitro inhibited M1 polarization, promoted M2 polarization, and improved cell viability.
Conclusions:
- TSPO plays a neuroprotective role in CIRI by inhibiting M1 microglia polarization and promoting M2 polarization.
- TSPO represents a potential therapeutic target for stroke treatment.
