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Anti-atherosclerotic Effect of the Methanol Extract of Sorbus commixta Cortex in the High Cholesterol-Diet Rats
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  • Anti-atherosclerotic Effect of the Methanol Extract of Sorbus commixta Cortex in the High Cholesterol-Diet Rats
  • Anti-atherosclerotic Effect of the Methanol Extract of Sorbus commixta Cortex in the High Cholesterol-Diet Rats
저자명
Kang. Dae-Gill,Sohn. Eun-Jin,Kim. Jin-Sook,Lee. Yun-Jung,Moon. Mi-Kyoung,Lee. An-Sook,An. Jun-Seok,Lee. Ho-Sub
간행물명
동의생리병리학회지
권/호정보
2006년|20권 5호|pp.1337-1345 (9 pages)
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대한동의생리학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Hypercholesterolemia is a pivotal pathogenic factor for the development and maintenance of atherosclerosis. The present study was designed to evaluate whether the methanol extract of Sorbus commixta cortex (MSC) restores vascular dysfunction in association with the aortic expressions of proinflarnmatory and adhesion molecules in high cholesterol (HC) diet-rats. Chronic treatment with low (100 mg/kg/day) or high doses (200 mg/kg/day) of MSC lowered the increase in plasma levels of triglyceride (TG) and low-density lipoprotein (LDL) cholesterol induced by a cholesterol-enriched diet without affecting on the plasma level of high density lipoprotein (HDL)-cholesterol. Vascular tone attenuated in the HC-diet rats was restored by administration with MSC. Treatment with MSC also suppressed the HC-induced increase in the monocyte chemoattractant protein-1 (MCP-1) and nuclear factor-$_K$B (NF-$_K$B) p65 expressions as well as expressions levels of adhesion molecules including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (ICAM-1), and E-selectin in aorta. The present study also showed that MSC inhibited the HC-mediated induction of ET-1 and ACE expression. In histopathological examination, aortic segments in the HC-diet rat revealed thickening intima and media, which were blocked by administration with MSC. Taken together, MSC could suppress the development of atherosclerosis in the HC-diet rat model through the inhibition of the aortic expression levels of pro-inflammatory and adhesion molecules.