A Novel Ultrafiltrate Extract of Propolis Exerts Anti‐inflammatory Activity through Metabolic Rewiring

Author:

Wu Yong‐Lin12,Zhu An‐Qi12,Zhou Xiao‐Ting12,Zhang Ke‐Wei12,Yuan Xu‐Jiang3,Yuan Min12,He Jian4,Pineda Miguel A.5,Li Kun‐Ping12ORCID

Affiliation:

1. Institute of Chinese Medicinal Sciences Guangdong TCM Key Laboratory for Metabolic Diseases Guangdong Pharmaceutical University Guangzhou 510006 China

2. Institute of Chinese Medicinal Sciences Guangdong Pharmaceutical University 280 East Road, Outer Ring, Guangzhou Higher Education Mega Center Guangzhou China 510006

3. Center for Drug Research and Development Guangdong Pharmaceutical University Guangzhou 510006 China

4. BYHEALTH Institute of Nutrition & Health. Guangzhou 510000 China

5. Centre for the Cellular Microenvironment University of Glasgow University Place Glasgow G12 8TA UK

Abstract

AbstractThousands of years ago, humans started to use propolis because of its medicinal properties, and modern science has successfully identified several bioactive molecules within this resinous bee product. However, a natural propolis extract which has been removed the adhesive glue and preserved propolis bioactive compounds is urgently needed to maximise the therapeutic opportunities. In this study, a novel ultrafiltrate fraction from Brazilian green propolis, termed P30K, was demonstrated with anti‐inflammatory properties, both in vitro and in vivo. Total flavonoids and total phenolic acids content in P30K were 244.6 mg/g and 275.8 mg/g respectively, while the IC50 value of inhibition of cyclooxygenase‐2 (COX‐2) was 8.30 μg/mL. The anti‐inflammatory activity of P30K was furtherly corroborated in experimental models of lipopolysaccharides (LPS)‐induced acute liver and lung injury. Mechanistically, integrated GC−MS and LC−MS based serum metabolomics analysis revealed that P30K modulated citrate cycle (TCA), pyruvate, glyoxylate and dicarboxylate metabolism pathways to inhibit secretion of pro‐inflammatory cytokines. Results of network pharmacology and molecular docking suggested that P30K targeted catechol‐O‐methyltransferases (COMT), 11β‐hydroxysteroid dehydrogenases (HSD11B1), and monoamine oxidases (MAOA and MAOB) to promote cellular metabolomic rewiring. Collectively, our work reveals P30K as an efficient therapeutic agent against inflammatory conditions and its efficacy is related to metabolic rewiring.

Funder

Natural Science Foundation of Guangdong Province

Publisher

Wiley

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