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已发表论文
Gbp2 表达下调通过抑制 STAT1 减轻脂多糖诱导的 BV2 小胶质细胞炎症反应
Authors Bao Y, Ni H, Wang K, Ma L, Gu J, Zhang X, Gao H, He G
Received 29 March 2025
Accepted for publication 9 September 2025
Published 6 October 2025 Volume 2025:18 Pages 13869—13877
DOI https://doi.org/10.2147/JIR.S531241
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Dharmappa Krishnappa
Yang Bao,1,2,* Hongwei Ni,1,2,* Kai Wang,1,* Limin Ma,1 Jiaqiu Gu,1 Xinxin Zhang,1 Hongmei Gao,1 Guangbao He1
1Department of Anesthesiology, Jiading District Central Hospital Affiliated Shanghai University of Medicine and Health Sciences, Shanghai, 201800, People’s Republic of China; 2Department of Anesthesiology, Jiading Hospital of Traditional Chinese Medicine, Shanghai, 201800, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Guangbao He, Jiading District Central Hospital Affiliated Shanghai University of Medicine and Health Sciences, Shanghai, 201800, People’s Republic of China, Email 13621953945@163.com
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.
Keywords: postoperative cognitive dysfunction, STAT1, Gbp2, neuroinflammation
1Department of Anesthesiology, Jiading District Central Hospital Affiliated Shanghai University of Medicine and Health Sciences, Shanghai, 201800, People’s Republic of China; 2Department of Anesthesiology, Jiading Hospital of Traditional Chinese Medicine, Shanghai, 201800, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Guangbao He, Jiading District Central Hospital Affiliated Shanghai University of Medicine and Health Sciences, Shanghai, 201800, People’s Republic of China, Email 13621953945@163.com
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.
Keywords: postoperative cognitive dysfunction, STAT1, Gbp2, neuroinflammation