논문번호 | 116 | ||
논문제목(영문) | Gallic Acid Inhibits Proliferation and Migration of Smooth Muscle Cells in a Pig In-Stent Restenosis Model. | ||
국내외구분 | 국내 | SCI여부 | KCI |
연구책임자역할 | 공저자 | ||
주저자명 | Kim HB | ||
교신저자명 | Hong YJ, | ||
공동저자명 | Lee SH, Kee HJ, Kim M, Ahn Y, Jeong MH | ||
게제년월일 | 2024-01-01 | ||
ISSN | 2233-7385 | ||
Impact Factor | 0 | ||
학술지명 | Chonnam Med J | ||
서지사항 | 0집 / 60권 / 1호, 페이지(32 - 39) | ||
요약초록문 (Abstract) 입력 |
In-stent restenosis (ISR) develops primarily due to neointimal hyperplasia. Gallic acid (GA) has anti-inflammatory, antioxidant, and cardioprotective effects. This study sought to investigate the effects of GA on neointimal hyperplasia and proliferation and migration of vascular smooth muscle cells (VSMCs) in a pig ISR model. In vitro proliferation and migration experiments were confirmed, after VSMCs were treated with platelet-derived growth factor (PDGF-BB) and GA (100 µM) using a 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay and a scratch wound assay for 24 hours and 48 hours. A bare metal stent (BMS) was implanted in the pig coronary artery to induce ISR with overdilation (1.1-1.2:1), and GA (10 mg/kg/day) was administered for 4 weeks. At the 4-week follow-up, optical coherence tomography (OCT) and histopathological analyses were performed. GA decreased the proliferation of VSMCs by PDGF-BB for 24 hours (89.24±24.56% vs. 170.04±19.98%, p<0.001) and 48 hours (124.87±7.35% vs. 187.64±4.83%, p<0.001). GA inhibited the migration of VSMCs induced by PDGF-BB for 24 hours (26.73±2.38% vs. 65.38±9.73%, p<0.001) and 48 hours (32.96±3.04% vs. 77.04±10.07%, p<0.001). Using OCT, % neointimal hyperplasia was shown to have significantly decreased in the GA group compared with control vehicle group (28.25±10.07% vs. 37.60±10.84%, p<0.001). GA effectively reduced neointimal hyperplasia by inhibiting the proliferation and migration of VSMCs in a pig ISR model. GA could be a potential treatment strategy for reducing ISR after stent implantation. | ||
파일 |
B116.pdf (9.6M) DATE : 2024-06-18 07:26:22 |
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