2. Academic Validation
  3. Fucoxanthin prevents septic cardiomyopathy by targeting BRD2 in M1-polarized macrophages

Fucoxanthin prevents septic cardiomyopathy by targeting BRD2 in M1-polarized macrophages

  • Food Funct. 2026 Jan 5. doi: 10.1039/d5fo04244e.
Xuechun Sun 1 2,  Tingwei Chen 1 2,  Xiqing Zhang 1,  Huali Meng 1 2,  Yanqi Hu 3,  Fang Zheng 3,  Yufeng Chu 4 5,  Lei Sun 6,  Hao Wu 1 2
Affiliations

Affiliations

  • 1 Department of Nutrition and Food Hygiene, School of Public Health, Cheeloo College of Medicine, Shandong University, 44 Wenhuaxi Rd., Jinan, Shandong 250012, China. [email protected].
  • 2 Shandong Provincial Engineering and Technology Research Center for Food Safety Monitoring and Evaluation, 44 Wenhuaxi Rd., Jinan, Shandong 250012, China.
  • 3 Cigar Business Center, China Tobacco Shandong Industrial Co. Ltd, 11888 Jingshi Rd., Jinan, Shandong 250100, China. [email protected].
  • 4 Neurocritical Care Unit, Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, China. [email protected].
  • 5 Shandong Provincial Hospital, Shandong University, 324 Jingwu Rd., Jinan, Shandong 250012, China.
  • 6 Department of Endocrinology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Wenhua Xi Rd., Jinan, Shandong 250012, China. [email protected].
PMID: 41489867 DOI: 10.1039/d5fo04244e
Abstract

Septic cardiomyopathy (SCM) leads to heart failure, with few effective approaches for its intervention. Fucoxanthin (FX) possesses anti-inflammatory capacity, but its effect on SCM remains unknown. Herein, we report that FX protects against cardiac dysfunction in a lipopolysaccharide (LPS)-induced mouse model of sepsis with a dramatic reduction of inflammatory cell infiltration in the heart tissue. The analysis of human and mouse databases revealed M1-polarized macrophages as the most evidently infiltrated immune cells into the heart tissue under septic conditions. This phenomenon was found in the current mouse model, which was significantly inhibited by FX. FX blunted macrophage M1 polarization in vitro that provoked inflammation in cardiomyocytes. Further, bromodomain-containing protein 2 (BRD2) was predicted as a molecular target of FX. Moreover, FX decreased BRD2 protein in both mouse hearts and macrophages in the presence of LPS. BRD2 overexpression abolished FX's macrophage-silencing effect. Notably, FX decreased BRD2 levels and inhibited inflammation in peripheral monocyte-derived macrophages from patients with SCM. The present study offers FX and BRD2 as a novel approach and molecular target for SCM intervention.

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