Work

Downregulation of Gbp2 Attenuates LPS-Induced Inflammation in BV2 Microglia Cells Through Inhibition of STAT1

Year: 2025

Type: article

Abstract: Introduction: Postoperative cognitive dysfunction (POCD) commonly occurs in around 50% of patients within first few weeks after surgery. Research indicates that the activation of microglia is believed to be closely associated with the decline in POCD. Neuroinflammation has been confirmed as a significant feature of POCD. Methods: Inflammation-associated differentially expressed genes (DEGs) were screened using GEO databases. Quantitative PCR and Western blot were applied for analysis of mRNA and protein expressions, respectively. Furthermore, the concentrations of IL-6 and TNF-α were measured using ELISA. Results: Six hippocampal tissues collected from three mice with POCD and three control mice were used for inflammation-associated differential gene expression analysis. In addition, Gbp2 was found to be significantly upregulated, which was associated with the inflammatory responses in patients with POCD. Knockdown of Gbp2 significantly reversed LPS-induced inflammation and apoptosis in mouse microglial BV2 cells. The anti-apoptotic and anti-inflammatory effects of Gbp2 deficiency was mediated by the transcription factors STAT1 and Irf1. Taken together, our findings demonstrated Gbp2 level was highly expressed in POCD patients comparing with that in non-POCD patients post-surgery. Conclusion: Downregulation of Gbp2 attenuates LPS-induced inflammation in BV2 cells through inhibition of STAT1, which might shed new lights on exploring new strategies against POCD.

Source: Journal of Inflammation Research

DOI: 10.2147/jir.s531241