고농도 U-46619에 의한 혈관의 수축에 대한 Resveratrol의 억제 작용에서 MEK 활성 또는 Rho-kinase 활성의 변화 : 내피 비의존적 수축성 조절

• 영문명: The Effect of Resveratrol on U-46619 (High Concentration)-induced Vasoconstriction Regulating MEK or Rho-kinase Activity
• 발행기관: 대한약학회
• 저자명: 제현동(Hyun Dong Je)
• 간행물 정보: 『약학회지』제55권 제2호 (2011년), 138~144쪽, 전체 7쪽
• 주제분류: 의약학 > 기타의약학
• 파일형태: PDF
• 발행일자: 2011.04.30

영문 초록

The aim of present study was to investigate the possible influence and related mechanism of resveratrol on U-46619 (high concentration)-induced vasoconstriction. Agonist-induced vascular smooth muscle contractions involve the activation of thick or thin filament pathway. However, there are no reports addressing the question whether this pathway is involved in resveratrol-induced relaxation in rat aortae contracted with high U-46619. We hypothesized that MEK or Rho-kinase inhibition plays a role in vascular relaxation evoked by resveratrol in rat aortae. Endothelium-denuded arterial rings from male Sprague-Dawley rats were used and isometric contractions were recorded using a computerized data acquisition system. Resveratrol fully inhibited U-46619 in low concentration-induced contraction regardless of endothelial function. However, resveratrol partially decreased U-46619 in high concentration- induced contraction regardless of endothelial function. Interestingly, only in U-46619 (high concentration)-induced contraction, no significant decrease was observed in phospho-ERK1/2 levels and slight decrease in phospho-MYPT1 levels suggesting that additional pathways different from them or endothelial nitric oxide synthesis might be involved in the vasorelaxation. In conclusion, in high U-46619-contracted rat aortae, resveratrol showed relaxation response regardless of endothelial function significantly but slightly decreasing MYPT1 phosphorylation rather than ERK1/2 phosphorylation.

키워드

ERK MEK resveratrol Rho-kinase vasoconstriction