Chlorogenic acid and quercetin alleviate food allergy responses through the PPAR-γ signaling pathway in mice.

Abstract

BACKGROUND: Food allergy has become a global public health problem. This study established a BALB/c mouse food allergy model to investigate the possible therapeutic effects of two widely studied polyphenols: chlorogenic acid (CA) and quercetin (QR). RESULTS: Compared to the positive allergic group, levels of IgE and IgG1 significantly reduced in the CA and QR treatment groups compared to the positive allergic group, while IgG2a levels showed a significant increase (P&#x2009;<&#x2009;0.05). Furthermore, compared with the positive allergic group, interleukin (IL)-4 levels were notably reduced by 11.62% and 29.02% in the CA and QR groups, whereas interferon-&#x3b3;, IL-10, and transforming growth factor-&#x3b2; levels were significantly higher than those in the allergic group (P&#x2009;<&#x2009;0.05). Additionally, histamine levels were markedly decreased by 33.94% and 49.31% in the CA and QR groups compared to the allergic group (P&#x2009;<&#x2009;0.05). Histopathological examination demonstrated considerable improvement in intestinal damage repair and a substantial reduction in mast cell degranulation following CA and QR treatments. Notably, the QR group showed nearly complete absence of intestinal inflammatory response. Subsequent reverse transcription quantitative polymerase chain reaction and western blot analysis indicated significant elevation in mRNA expression levels of IL-10 and forkhead box protein P3 (FOXP3) in the jejunum of mice (P&#x2009;<&#x2009;0.05), along with notable enhancement in the protein expression levels of peroxisome proliferator-activated receptor &#x3b3; (PPAR-&#x3b3;), cluster of differentiation 36 (CD36) and carnitine palmitoyltransferase 1 (CPT1) (P&#x2009;<&#x2009;0.05), elucidating the mechanism by which CA and QR alleviated allergic reactions. CONCLUSION: The typical polyphenols CA and QR alleviated food allergy responses in mice by boosting PPAR-&#x3b3; activity, which upregulated CD36/CPT1-mediated fatty acid oxidation. &#xa9; 2025 Society of Chemical Industry.