Department of Emergency Medicine, Shin Kong Wu Ho-Su Memorial Hospital , Taipei, Taiwan.
J Agric Food Chem. 2014 Feb 12;62(6):1213-20. doi: 10.1021/jf404479x. Epub 2014 Jan 28.
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.
瘦素参与血管修复和心血管事件的发病机制。本研究评估了 EGCG 在球囊损伤诱导瘦素表达中的分子机制。根据免疫组织化学和共聚焦分析，瘦素表达增加，球囊损伤后主动脉腔变窄。EGCG 治疗可减轻瘦素表达并减少新生内膜形成。体外研究表明，血管紧张素 II（Ang II）诱导培养的血管平滑肌细胞（VSMCs）迁移和增殖，而 EGCG、瘦素 siRNA 和 c-Jun siRNA 治疗可显著抑制 VSMCs 的迁移和增殖。EMSA 显示球囊损伤增加了 AP-1 结合活性，而 EGCG 和 c-Jun siRNA 抑制了 AP-1 结合活性。Western blot 和实时 RT-PCR 分析在血管内膜组织样本中得到了类似的结果。总之，球囊损伤诱导大鼠颈动脉中瘦素表达，而 EGCG 通过 JNK/AP-1 通路抑制瘦素表达，并减轻新生内膜形成。
