Open AccessHigh glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line
Author(s) -
Hung HaoChang,
Tsai ShengFeng,
Sie ShihRen,
Kuo YuMin
Publication year - 2022
Publication title -
immunity, inflammation and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 18
ISSN - 2050-4527
DOI - 10.1002/iid3.610
Subject(s) - microglia , neuroinflammation , tlr4 , inflammation , p38 mitogen activated protein kinases , lipopolysaccharide , microbiology and biotechnology , nitric oxide synthase , signal transduction , phosphorylation , immune system , nitric oxide , kinase , biology , cancer research , immunology , chemistry , endocrinology , protein kinase a
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.