Sohn Eun Jin, Kang Dae Gill, Mun Yeun Ja, Woo Won Hong, Lee Ho Sub
Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, Korea.
Biol Pharm Bull. 2005 Aug;28(8):1444-9. doi: 10.1248/bpb.28.1444.
The present study was designed to examine whether the methanol extract of Sorbus commixta cortex (MSC) could prevent the development of atherosclerosis through regulating the vascular nitric oxide (NO) and endothelin-1 (ET-1) systems in atherogenic-diet rats. Our findings show that aortic NO production as well as endothelial nitric oxide synthase (ecNOS) expression was significantly decreased in atherogenic-diet rats compared with those in the control group. Aortic ET-1 expression was augmented in rats fed an atherogenic-diet while NF-kappaB p65 was upregulated. Treatment of atherogenic-diet rats with either low (100 mg/kg/d) or high (200 mg/kg/d) doses of MSC led not only to significant increases in the aortic NOS/NO system, but also to decreases in aortic ET-1 expression. The aortic expression level of NF-kappaB p65 was also attenuated in atherogenic-diet rats by chronic treatment with low or high doses of MSC. Atherogenic-diet induced increases in the expression of adhesion molecules including intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin were markedly decreased by treatment with MSC. From the histopathological examination, MSC treatment was shown to lessen the thickening noted in the aortic intima and media of the atherogenic-diet rats. These results suggest that MSC affects the atherogenic process via the suppression of proinflammatory and adhesion molecules in atherogenic-diet rats, which may be, at least in part, causally related with the regulation of vasoactive systems such as the NO and ET-1 systems.
本研究旨在探讨花楸树皮甲醇提取物（MSC）是否能通过调节致动脉粥样硬化饮食大鼠的血管一氧化氮（NO）和内皮素-1（ET-1）系统来预防动脉粥样硬化的发展。我们的研究结果表明，与对照组相比，致动脉粥样硬化饮食大鼠的主动脉NO生成以及内皮型一氧化氮合酶（ecNOS）表达显著降低。喂食致动脉粥样硬化饮食的大鼠主动脉ET-1表达增加，而核因子κB p65上调。用低剂量（100 mg/kg/d）或高剂量（200 mg/kg/d）的MSC处理致动脉粥样硬化饮食大鼠，不仅导致主动脉NOS/NO系统显著增加，还导致主动脉ET-1表达降低。通过低剂量或高剂量的MSC长期处理，致动脉粥样硬化饮食大鼠主动脉中核因子κB p65的表达水平也有所减弱。用MSC处理可显著降低致动脉粥样硬化饮食诱导的包括细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）和E-选择素在内的黏附分子表达增加。组织病理学检查显示，MSC处理可减轻致动脉粥样硬化饮食大鼠主动脉内膜和中膜的增厚。这些结果表明，MSC通过抑制致动脉粥样硬化饮食大鼠中的促炎和黏附分子来影响动脉粥样硬化进程，这可能至少部分与调节血管活性系统如NO和ET-1系统有因果关系。
