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.
The type II variant of Kounis syndrome is defined as a rare allergic myocardial angina or infarction event in patients with preexisting quiescent coronary artery disease. Various causative factors have been implicated in the etiology of Kounis syndrome. However, reports highlighting the importance of recognizing a decreased preload caused by allergic right ventricular (RV) myocardial infarction and subsequent cardiogenic shock from ongoing anaphylactic shock are rare. Here we report the case of a 54-year-old male who initially presented with anaphylactic shock after ingesting onions. His condition silently progressed to RV infarction and cardiogenic shock within 2 hours of symptom onset. Under such instances, it is crucial to promptly identify RV infarction and cardiogenic shock by repeatedly performing electrocardiography at frequent intervals.
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