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Updated: Sep 23, 2026
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
Sult2b1 Modulates NLRP3/BCL-2 Signaling and Pro-Inflammatory Microglial/Macrophage Polarization After Traumatic Brain
Hao Zhang1, Zhenhong Pan1, Hua Chen2
1Department of Neurosurgery, Fuzong Clinical Medical College of Fujian Medical University, Fuzhou, Fujian Province, China.
Introduction:
Traumatic Brain Injury (TBI) causes prolonged neurological impairment through primary mechanical damage and secondary cascades including neuroinflammation and apoptosis. This study investigated whether Sult2b1, a cholesterol sulfation enzyme, protects against secondary injury after TBI.
Methods:
A Controlled Cortical Impact (CCI) mouse model was used. Sult2b1 expression was assessed by RT-qPCR and western blotting. AAV-mediated delivery restored Sult2b1, and its effects were evaluated via histology, immunofluorescence, imaging, ELISA, and behavioral tests.
Results:
Sult2b1 was markedly downregulated after TBI. Overexpression improved cerebral blood flow, preserved neurons, reduced apoptosis, decreased TNF-α and IL-1β, and increased IL-4. Mechanistically, it modulated NLRP3/BCL-2 and suppressed M1-like microglial/macrophage polarization. Functionally, it enhanced sensorimotor and cognitive performance and reduced lesion volume and chronic tissue loss.
Discussion:
Our findings identify Sult2b1 as an endogenous protective factor that limits neuroinflammation and promotes neuronal survival via NLRP3/BCL-2 and microglial polarization modulation, suggesting therapeutic potential.
Conclusion:
Sult2b1 confers neuroprotection after TBI and may serve as a potential target for reducing secondary brain injury.
