High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line. Issue 5 (19th April 2022)

• Record Type: Journal Article
• Authors: Hung, Hao‐Chang; Tsai, Sheng‐Feng; Sie, Shih‐Ren; Kuo, Yu‐Min
• Is Part Of: Immunity, inflammation and disease. Volume 10:Issue 5(2022)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-04-19
• Subjects: diabetes -- neuroinflammation -- NF‐κB -- p38 -- TLR4; Immunology -- Periodicals; Immunity -- Periodicals; Inflammation -- Periodicals; 616.079
• DOI: 10.1002/iid3.610
• Languages: English
• ISSNs: 2050-4527

Abstract

Abstract: Introduction: Diabetes mellitus emerges as a global health crisis and is related to the development of neurodegenerative diseases. Microglia, a population of macrophages‐like cells, govern immune defense in the central nervous system. Activated microglia are known to play active roles in the pathogenesis of neurodegenerative diseases. Methods: This study aimed to investigate the effects of high glucose on low‐dose lipopolysaccharide (LPS)‐induced activations of inflammation‐related signaling molecules in cultured BV2 microglial cells. Results: Compared to cells cultured in the normal glucose medium (NGM, 5.5 mM), the LPS‐induced activation of NF‐κB lasted longer in cells cultured in high glucose medium (HGM, 25 mM). HGM also enhanced the expression of inducible nitric oxide synthase (iNOS). Among the mitogen‐activated protein kinases, HGM enhanced the LPS‐induced phosphorylation of p38 without affecting the phosphorylation of Erk1/2 or JNK. BV2 cells cultured in HGM expressed higher levels of TLR4 than those cells cultured in NGM. Conclusion: High glucose aggravated LPS‐induced inflammatory responses of microglia via enhancing the TLR4/p38 pathway and prolonging the activation of NF‐κB/iNOS signaling. Controlling blood glucose levels is advised to manage neuroinflammation and related neurodegenerative diseases. Abstract : High glucose prolongs LPS‐induced phosphorylation of NF‐kB.