BPB Reports

Paper Details

BPB Reports
Vol. 9 No. 4 p.89-93 2026
Report
Cyanidin-3-Glucoside Attenuates aP2 Expression Independent of PPRE-Mediated Transcription in Macrophage Cells
  • Atsuko Masumi (Department of Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Aomori University / Miyagi Gakuin Woman’s University / amasumi2175@gmail.com)
Ayato Kokabu 1) 2) , Iroha Yodogawa 5) , Masahiko Ito 4) , Katsuyoshi Kamiie 3) , Tetsurou Ikeda 2) , Atsuko Masumi 1) 5)
1) Department of Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Aomori University , 2) Department of Clinical Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Aomori University , 3) Department Molecular Biology, Faculty of Pharmaceutical Sciences, Aomori University , 4) Department of Microbiology and Immunology, Hamamatsu University School of Medicine , 5) Miyagi Gakuin Woman’s University
Received: May 25, 2026;   Accepted: July 14, 2026;   Released: July 24, 2026
Keywords: cyanidin-3-glucoside, anthocyanins, inflammation, RAW264.7, aP2, cytokines
Abstracts

Cyanidin-3-glucoside (C3G) is a major anthocyanin present in various berries and pigmented grains and has been reported to exhibit antioxidant and anti-inflammatory activities. In the present study, we examined the effects of C3G on inflammatory responses in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, with particular attention to adipocyte protein 2 (aP2), a lipid-associated protein implicated in inflammation. Treatment with C3G at concentrations up to 50 μM did not affect cell viability in the presence or absence of LPS. Quantitative real-time PCR analysis demonstrated that C3G significantly suppressed LPS-induced expression of aP2, as well as the pro-inflammatory cytokines monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6). Furthermore, luciferase reporter assays revealed that C3G inhibited LPS-induced aP2 promoter activity in a manner independent of the peroxisome proliferator-activated receptor response element (PPRE)-like site. These findings indicate that C3G attenuates macrophage inflammatory responses through the suppression of aP2 expression and pro-inflammatory cytokine production, suggesting a novel molecular basis for the anti-inflammatory action of C3G.