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High glucose enhances lipopolysaccharide-induced inflammation in cultured BV2 microglial cell line

Hao-Chang Hung1, Sheng-Feng Tsai2,3, Shih-Ren Sie4

  • 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Immunity, Inflammation and Disease
|April 28, 2022
PubMed
Abstract

Insights

High glucose worsens microglial inflammation, a key factor in neurodegenerative diseases. This occurs through the TLR4/p38 pathway and prolonged NF-κB/iNOS signaling, highlighting the need for blood glucose control.

Area of Science:

  • Neuroscience
  • Immunology
  • Endocrinology

Background:

  • Diabetes mellitus is a global health crisis linked to neurodegenerative diseases.
  • Microglia are key immune cells in the central nervous system, implicated in neurodegeneration pathogenesis.

Purpose of the Study:

  • To investigate the impact of high glucose on microglial inflammatory signaling pathways.
  • To understand how high glucose affects lipopolysaccharide (LPS)-induced microglial activation.

Main Methods:

  • Utilized cultured BV2 microglial cells.
  • Exposed cells to normal glucose medium (NGM) and high glucose medium (HGM).
  • Stimulated cells with low-dose lipopolysaccharide (LPS) and analyzed inflammatory signaling molecules.

Main Results:

  • High glucose prolonged LPS-induced NF-κB activation and enhanced inducible nitric oxide synthase (iNOS) expression.
  • High glucose increased LPS-induced p38 MAPK phosphorylation, but not Erk1/2 or JNK.
  • BV2 cells in high glucose exhibited higher Toll-like receptor 4 (TLR4) levels.

Conclusions:

  • High glucose exacerbates LPS-induced microglial inflammation via the TLR4/p38 pathway and prolonged NF-κB/iNOS signaling.
  • Controlling blood glucose is crucial for managing neuroinflammation and associated neurodegenerative diseases.
Keywords:
NF-κBTLR4diabetesneuroinflammationp38

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