Total glucosides of paeony alleviates cGAS-STING-mediated diseases by blocking the STING-IRF3 interaction

Chin J Nat Med. 2024 May;22(5):402-415. doi: 10.1016/S1875-5364(24)60572-8.

Abstract

In the realm of autoimmune and inflammatory diseases, the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) signaling pathway has been thoroughly investigated and established. Despite this, the clinical approval of drugs targeting the cGAS-STING pathway has been limited. The Total glucosides of paeony (TGP) is highly anti-inflammatory and is commonly used in the treatment of rheumatoid arthritis (RA), emerged as a subject of our study. We found that the TGP markedly reduced the activation of the cGAS-STING signaling pathway, triggered by various cGAS-STING agonists, in mouse bone marrow-derived macrophages (BMDMs) and Tohoku Hospital Pediatrics-1 (THP-1) cells. This inhibition was noted alongside the suppression of interferon regulatory factor 3 (IRF3) phosphorylation and the expression of interferon-beta (IFN-β), C-X-C motif chemokine ligand 10 (CXCL10), and inflammatory mediators such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The mechanism of action appeared to involve the TGP's attenuation of the STING-IRF3 interaction, without affecting STING oligomerization, thereby inhibiting the activation of downstream signaling pathways. In vivo, the TGP hindered the initiation of the cGAS-STING pathway by the STING agonist dimethylxanthenone-4-acetic acid (DMXAA) and exhibited promising therapeutic effects in a model of acute liver injury induced by lipopolysaccharide (LPS) and D-galactosamine (D-GalN). Our findings underscore the potential of the TGP as an effective inhibitor of the cGAS-STING pathway, offering a new treatment avenue for inflammatory and autoimmune diseases mediated by this pathway.

Keywords: Inflammation; LPS/D-GalN; STING inhibitor; Total glucosides of gaeony; cGAS-STING pathway.

MeSH terms

  • Animals
  • Glucosides* / pharmacology
  • Humans
  • Interferon Regulatory Factor-3* / metabolism
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Membrane Proteins* / genetics
  • Membrane Proteins* / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Nucleotidyltransferases* / genetics
  • Nucleotidyltransferases* / metabolism
  • Paeonia* / chemistry
  • Signal Transduction* / drug effects
  • THP-1 Cells

Substances

  • Interferon Regulatory Factor-3
  • Membrane Proteins
  • Glucosides
  • Nucleotidyltransferases
  • Sting1 protein, mouse
  • Irf3 protein, mouse
  • STING1 protein, human
  • cGAS protein, mouse