| Summary: | 碩士 === 國立臺灣師範大學 === 人類發展與家庭學系 === 95 === Atherosclerosis is characterized by accumulation of lipids, inflammatory cell, and connective tissue within the arterial wall. It is a chronic, progressive disease with a long asymptomatic phage. Macrophages are involved in every phase of atherogenesis. Research suggests that wild bitter gourd decreases the release of pro-inflammatory mediator PGE2 and nitric oxide （NO）. The aim of this study was to investigate the effect of ethyl acetate extracts（EAE）of wild bitter gourd（Momordica charantia L.）, saponifiable substances of ethyl acetate（S）and nonsaponification of ethyl acetate（NS）on Lipopolysaccharide（LPS）-stimulated RAW 264.7 macrophages. The results showed（1）2381EAE, 2381NS and 2381S decreased NO production and iNOS expression in a dose-dependent manner（p＜0.05）.TNF-α production reduced significantly by 2381EAE（300 μg/ml）.There were no significant changes in TNF-α production with 2381NS or 2381S. IL-10 production was not changed by 2381EAE or 2381NS, but was significantly decreased by 2381S（250-300 μg/ml）（p＜0.05）.（2）CK-EAE（200 - 300 μg/ml）and CK-S（150 μg/ml）significantly decreased NO production and iNOS expression, but CK-NS did not. TNF-α and IL-10 releases were not significantly changed by CK extracts. To test the effect of bitter gourd in vivo metabolites on macrophages, serum samples（EAE serum）obtained from ICR mice fed diet containing 1.5% 2381EAE for 1 week were used to culture RAW 264.7 macrophage. The results showed that NO and TNF-α production were not significantly different between EAE-serum and baseline-serum treatments. But, IL-10 secretion increased significantly in macrophages cultured with EAE-serum（p＜0.05）. Capric acid and conjugated linolenic acid (CLN), identified from bitter gourd to be a PGE2 inhibitor of macrophage, and a PPAR-alpha activator, respectively, and fenofibrate, a well-known PPAR-alpha activator, were also investigated in this model. The results showed fenofibrate, capric acid and CLN decreased nitric oxide production without statistical significance, but the expression of iNOS was down regulated by all of them. TNF-α production in cells incubated with fenofibrate decreased by 26.5% while that with capric acid increased as compared with cells incubated with LPS alone. IL-10 productions were not significantly changed by fenofibrate, capric acid or CLN. In conclusion, the wild bitter gourd EAE decreases the productions of inflammatory mediator NO and TNF, and the bio-metabolites of bitter gourd EAE increase the production of anti-inflammatory mediator IL-10 in macrophages.
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