2. Academic Validation
  3. Equisetin protects from atherosclerosis in vivo by binding to STAT3 and inhibiting its activity

Equisetin protects from atherosclerosis in vivo by binding to STAT3 and inhibiting its activity

  • Pharmacol Res. 2024 Aug:206:107289. doi: 10.1016/j.phrs.2024.107289.
Yuting Yang 1,  Jingzhu Wang 1,  Yang Tian 1,  Min Li 1,  Shaohua Xu 1,  Lijun Zhang 2,  Xiaowei Luo 3,  Yanhui Tan 4,  Hong Liang 5,  Ming Chen 6
Affiliations

Affiliations

  • 1 State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China.
  • 2 State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China; GXNU & GLHCWM Joint Medical Research Center, Guangxi Normal University, Guilin 541004, China.
  • 3 Institute of Marine Drugs, Guangxi University of Chinese Medicine, Nanning 530200, China.
  • 4 State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China. Electronic address: thy533@126.com.
  • 5 State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China. Electronic address: hliang@gxnu.edu.cn.
  • 6 State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Collaborative Innovation Center for Guangxi Ethnic Medicine, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China; GXNU & GLHCWM Joint Medical Research Center, Guangxi Normal University, Guilin 541004, China. Electronic address: chenmingprotein@mailbox.gxnu.edu.cn.
PMID: 38960011 DOI: 10.1016/j.phrs.2024.107289
Abstract

Atherosclerosis is a chronic inflammatory vascular disease characterized by lipid metabolism disorder and lipid accumulation. Equisetin (EQST) is a hemiterpene compound isolated from fungus of marine Sponge origin, which has Antibacterial, anti-inflammatory, lipid-lowering, and weight loss effects. Whether EQST has anti-atherosclerotic activity has not been reported. In this study, we revealed that EQST displayed anti- atherosclerosis effects through inhibiting macrophage inflammatory response, lipid uptake and foam cell formation in vitro, and finally ameliorated high-fat diet (HFD)-induced atherosclerosis in AopE-/- mice in vivo. Mechanistically, EQST directly bound to STAT3 with high-affinity by forming hydrophobic bonds at GLN247 and GLN326 residues, as well as hydrogen bonds at ARG325 and THR346 residues. EQST interacted with STAT3 physically, and functionally inhibited the transcription activity of STAT3, thereby regulating atherosclerosis. Therefore, these results supports EQST as a candidate for developing anti-atherosclerosis therapeutic agent.

Keywords

Atherosclerosis; EQST; Foam cell, Chemical compounds studied in this article Equisetin (PubChem CID: 54684703); Macrophage; Rosuvastatin (PubChem CID: 446157); STAT3.

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