Academic literature on the topic '不飽和脂肪酸'

LANGUAGE NOTE | Document text in English; abstract also in Chinese.
 There is growing interest in the potentially harmful effects in swimming pools, and the potential for swimming-related health hazards, which is gaining importance in competitive swimmers. This review was focused to discuss the following topics: (1) prevalence of respiratory difficulties in swimmers; (2) the possible factors and mechanisms which lead to the development of airway disorders in elite swimmers; (3) diet and nutrient supplementation for the management and prevention of airway problems. Summaries were concluded in this review according to the current knowledge of the respiratory problems in swimmers: (1) a high prevalence of respiratory symptoms and respiratory diseases in the elite swimmer population; (2) the potentially harmful effects in airway epithelial damage and lung permeability may caused by exposure in cold air, chlorinated products in swimming pools, and high intensity training in swimmers. (3) Observational studies have reported associations between airway symptoms and nutritional intervention (i.e. polyunsaturated fatty acid, dietary antioxidants, and vitamin D), which may have application for promoting health and sports performance for swimmers.
 運動選手(如游泳選手)發生呼吸系統疾病問題逐漸受到重視，本篇綜評旨在討論下列課題：(1)選手發生呼吸道疾病之發生率；(2)發生呼吸疾病之可能原因及機轉；(3)飲食與營養補充對減低呼吸疾病症狀之探討。統整相關文獻後，獲以下結語：(1)游泳選手發生呼吸道疾病之情形高於其他運動者(如：冬季運動項目、短跑與長跑等)；(2)長期處於含氯物質及其氯產物環境，對吸呼道黏膜及肺組織將有所傷，而冷空氣環境及高強度訓練模式，亦是增加游泳選手發生呼吸道不適症狀的影響因素；(3)多元不飽和脂肪酸、抗氧化物質及維生素D等營養素，在減低呼吸疾病臨床研究上證實有改善效益，對於呼吸道疾病發生率較高的游泳選手而言，應是不錯的飲食及營養補充介入不錯的選擇。

博士<br>國立陽明大學<br>生化暨分子生物研究所<br>101<br>Dietary supplementation of n-3 polyunsaturated fatty acids (n-3 PUFAs) has been reported to alleviate the symptoms of several chronic inflammatory diseases, such as atherosclerosis, rheumatoid arthritis and inflammatory bowel disease. Inhibition of the inflammatory factors expression has been considered to be one of the mechanisms that contribute to the beneficial effects of n-3 PUFAs. C-reactive protein (CRP), an acute phase protein in humans, is predominantly produced by hepatocytes in response to interleukin-6 (IL-6). Several epidemiological studies have reported that dietary intake of n-3 polyunsaturated fatty acids (n-3 PUFAs) is inversely associated with serum CRP concentration. However, the molecular mechanism by which n-3 PUFAs reduce the CRP level in hepatocytes remains unclear. The aims of this study were to examine the effect of the n-3 PUFAs, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), on the modulation of IL-6-induced CRP expression and to explore its possible mechanisms. We demonstrated that DHA and EPA inhibit IL-6-induced CRP protein and mRNA expression, as well as reduce CRP promoter activity in HepG2 cells. Knockdown of signal transducer and activator of transcription 3 (STAT3) and CCAAT box/enhancer-binding protein β (C/EBPβ) by short hairpin RNAs significantly decreased IL-6-induced CRP promoter activity. Our results showed that DHA and EPA decreased IL-6-induced STAT3 activity but not ERK1/2 and C/EBPβ activity. Furthermore, we found that nuclear protein tyrosine phosphatase (PTP) activity was up-regulated by DHA and EPA treatments. The inhibitiory effects of DHA and EPA on IL-6-induced STAT3 phosphorylation and CRP promoter activity were reversed by PTP inhibitor (Na3VO4). Form immunoprecipitation experiments, we observed that DHA and EPA induced the protein–protein interactions between STAT3 and TC-PTP. Taken together, our results demonstrate that DHA and EPA are able to reduce IL-6-induced CRP expression in HepG2 cells via an inhibition of STAT3 activation. We further show that DHA and EPA inhibit IL-6-induced STAT3 activation and CRP promoter activity through up-regulation of TC-PTP activation. Vascular endothelial cells are the primary target of immunological attack in inflammatory vascular diseases, and their injury can lead to the pathogenesis of atherosclerosis. During atherosclerotic progression, monocyte recruitment to the endothelium is enhanced by adhesion molecules on the surface of endothelial cells, including vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1). The cytokine-induced expression of cell adhesion molecules is regulated predominantly by activation of nuclear factor-κB (NF-κB) and activator protein-1 (AP-1). Experimental and clinical studies provide evidence that n-3 PUFAs are potential therapeutic agents for the prevention of inflammation and atherosclerosis. However, the mechanisms of n-3 PUFAs in the regulation of VCAM-1 and ICAM-1 expression in human aortic endothelial cells (HAECs) remain unclear. Another aim of this study was to investigate whether n-3 PUFAs regulate the adhesion molecules expression through NF-κB and AP-1 signaling pathways. We demonstrated that DHA inhibited THP-1 cell adhesion to tumor necrosis factor α (TNF-α)-activated HAECs. DHA significantly reduced VCAM-1 protein expression in TNF-α-treated HAECs, as determined by Western blot analysis. In line with NF-κB signaling pathway, DHA suppressed the TNF-α-activated IκBα phosphorylation and degradation as well as IκB kinase-β phosphorylation. Subsequently, nuclear translocation of the NF-κB (p50/p65) and AP-1 (c-Fos/c-Jun) subunits was down-regulated by DHA in HAECs. These results suggest that DHA decreases TNF-α-induced VCAM-1 expression through attenuation of NF-κB signaling pathway and AP-1 activation, and this may be important in the anti-inflammatory mechanism of DHA.