Mechanistic role of quercetin as inhibitor for adenosine deaminase enzyme in rheumatoid arthritis: systematic review

Cell Mol Biol Lett. 2024 Jan 16;29(1):14. doi: 10.1186/s11658-024-00531-7.

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease involving T and B lymphocytes. Autoantibodies contribute to joint deterioration and worsening symptoms. Adenosine deaminase (ADA), an enzyme in purine metabolism, influences adenosine levels and joint inflammation. Inhibiting ADA could impact RA progression. Intracellular ATP breakdown generates adenosine, which increases in hypoxic and inflammatory conditions. Lymphocytes with ADA play a role in RA. Inhibiting lymphocytic ADA activity has an immune-regulatory effect. Synovial fluid levels of ADA are closely associated with the disease's systemic activity, making it a useful parameter for evaluating joint inflammation. Flavonoids, such as quercetin (QUE), are natural substances that can inhibit ADA activity. QUE demonstrates immune-regulatory effects and restores T-cell homeostasis, making it a promising candidate for RA therapy. In this review, we will explore the impact of QUE in suppressing ADA and reducing produced the inflammation in RA, including preclinical investigations and clinical trials.

Keywords: Adenosine deaminase; Flavonoid; Quercetin; Rheumatoid arthritis; Synovial fluid.

Publication types

  • Systematic Review

MeSH terms

  • Adenosine
  • Adenosine Deaminase / metabolism
  • Adenosine Deaminase Inhibitors* / pharmacology
  • Arthritis, Rheumatoid* / drug therapy
  • Humans
  • Inflammation / drug therapy
  • Quercetin* / pharmacology

Substances

  • Adenosine
  • Adenosine Deaminase
  • Quercetin
  • Adenosine Deaminase Inhibitors