| Summary: | 碩士 === 中國文化大學 === 生物科技研究所 === 95 === Oxidative stress and inflammation are thought to be an important contributor and promoter of atherogenesis. While altered expression of cell adhesion molecules by the arterial endothelium plays a major role during atherogenesis and chronic inflammation. The pro-inflammatory cytokine TNF-α (tumor necrosis factor-alpha) could induce ICAM-1 (intercellular adhesion molecule-1) and VCAM-1 (vascular cell adhesion molecule-1) in atherogenesis through ROS activation. The aim of this study was to discuss the effect of chorophyll-related compounds (chlorophyll a+b, chlorophyll a, chlorophyll b and chorophyllin) on inflammatory response in TNF-α treated human aortic endothelial cells(HAEC). At 10μM chlorophyll a+b, chlorophyll a, chlorophyll b, and chorophyllin had no toxicity to HAEC. Chlorophyll a+b, chlorophyll a, chlorophyll b and chorophyllin inhibited the endothelial cell-leukocyte adhesion percentage up to 92.0±1%, 49.5±2.2%, 82.4±2.1% and 47.4±3.3%, respectively. At the same concentration of chlorophyll a+b, chlorophyll a, chlorophyll b, chorophyllin and Aspirin also significantly inhibited the expression of cell adhesion molecules, VCAM-1 and ICAM-1 by 46.6±3.2%, 50±2.2%, 51±2.5%, 30.2±2.1%, 44.1±1.3% and 30±2.1%, 32.6±1.3%, 51.3±3.2%, 13.5±2.3% , 28±3.3%, respectively. To conclusion, chorophyll-related compounds significantly inhibit TNF-αinduced the expression of cell adhesion molecules, VCAM-1 and ICAM-1. It may slow down inflammatory response, particularly in Chl a and Chl b treated groups.
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