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Protective effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats
Jiawei Fu1, Chunshuai Wu1, Guanhua Xu1
1The Affiliated Hospital 2 of Nantong University, Nantong University, The First People's Hospital of Nantong, Nantong 226001, Jiangsu, People's Republic of China; Key Laboratory for Restoration Mechanism and Clinical Translation of Spinal Cord Injury, Nantong 226001, Jiangsu, People's Republic of China; Research institute for Spine and spinal cord disease of Nantong University, 226001, Jiangsu, People's Republic of China.
Background:
Spinal cord injury (SCI) is a devastating disease that can lead to tissue loss and neurological dysfunction. TNIP2 is a negative regulator of NF-κB signaling due to its capacity to bind A20 and suppress inflammatory cytokines-induced NF-κB activation. However, the anti-inflammatory role of TNIP2 in SCI remains unclear. Our study's intention was to evaluate the effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats.
Methods:
HE staining and Nissl staining were performed on day 3 following SCI to analyze the histological changes. To further investigate the functional changes of TNIP2 after SCI, we performed immunofluorescence staining experiments. The effect of LPS on TNIP2 expression in BV2 cells was examined by western blot. The levels of TNF-α, IL-1β, and IL-6 in spinal cord tissues of rats with SCI and in BV2 cells with LPS were measured by using qPCR.
Results:
TNIP2 expression was closely associated with the pathophysiology of SCI in rats, and TNIP2 was involved in regulating functional changes in microglia. TNIP2 expression was increased during SCI in rats and that overexpression of TNIP2 inhibited M1 polarization and pro-inflammatory cytokine production in microglia, which might ultimately protect against inflammatory responses through the MAPK and NF-κB signaling pathways.
Conclusions:
The present study provides evidence for a role of TNIP2 in the regulation of inflammation in SCI and suggests that induction of TNIP2 expression alleviated the inflammatory response of microglia.
