Molecular mechanism of (-)-epigallocatechin-3-gallate on balloon injury-induced neointimal formation and leptin expression

Chiu Mei Lin, Sheng Wen Hou, Bao Wei Wang, Jiann Ruey Ong, Hang Chang, Kou-Gi Shyu

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


Leptin contributes to the pathogenesis of vascular repair and cardiovascular events. This study evaluated the molecular mechanism of EGCG in balloon injury-induced leptin expression. According to immunohistochemical and confocal analyses, leptin expression was increased and the aortic lumen exhibited narrowing after balloon injury. EGCG treatment attenuated leptin expression and diminished neointimal formation. The in vitro study showed that angiotensin II (Ang II) induced the migration and proliferation of cultured vascular smooth muscle cells (VSMCs), whereas treatment with EGCG, leptin siRNA, and c-Jun siRNA inhibited the migration and proliferation of VSMCs significantly. The EMSA shows that balloon injury increased AP-1-binding activity, and EGCG and c-Jun siRNA inhibited the AP-1-binding activity. Western blot and real-time RT-PCR analyses revealed similar results in intimal tissue samples. In summary, balloon injury induces leptin expression in the carotid artery of rats, and EGCG inhibits leptin expression through the JNK/AP-1 pathway and also attenuates neointimal formation.

Original languageEnglish
Pages (from-to)1213-1220
Number of pages8
JournalJournal of Agricultural and Food Chemistry
Issue number6
Publication statusPublished - Feb 12 2014


  • EGCG
  • angiotensin II
  • balloon injury
  • leptin
  • neointima formation

ASJC Scopus subject areas

  • General Chemistry
  • General Agricultural and Biological Sciences


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