Effects of the wild bitter gourd extracts on the inflammatory responses by a macrophage cell line

ASIA unversity > 醫學暨健康學院 > 食品營養與保健生技學系 > 博碩士論文 > Item 310904400/2889

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题名:	Effects of the wild bitter gourd extracts on the inflammatory responses by a macrophage cell line
作者:	chou you min
贡献者:	Department of Health and Nutrition Biotechnology?????
关键词:	Wild bitter gourd;Anti-inflammatory effects;PPARγ
日期:	2007
上传时间:	2009-11-16 08:07:59 (UTC+0)
出版者:	Asia University
摘要:	Wild bitter gourd (Cucurbitaceae) is an annual herbaceous vines climbing plant. It is also named wild balsam pear, short fruit bitter gourd or small bitter gourd, which crops from April to September. In traditional Chinese medical textbook, it already records definite efficacy for internally and externally application of wild bitter gourd. Recently, the scientific research showed that bitter gourd extracts could activate such as transcription factors PPAR (Peroxisome Proliferator-Activated Receptor). In the previous studies, activators of PPAR? may be potential in anti-diabetic, anti inflamanatory, anti-viral and anti-cancer related immunomodulation effects. Therefore, this study will focus on exploring the ethyl acetate extracts of wild bitter gourd?stem, leaf, flower and fruit? and juice of water soluble extracts on the inflammatory responses of related genes and proteins expression. Using different parts of wild bitter gourd extracts, respectively, RAW264.7 macrophage cells were treated with different concentrations ?10?50?100 ?g/mL?and LPS . The MTT assay results showed that wild bitter gourd extract treatments did not significantly influence the cell viability. Furthermore, transient transfection assay showed that extracts of wild bitter gourd residue at the concentration of 100 ?g/mL activated PPAR?. Inflammatory mediators such as PGE2 and NO2 showed that extracts of wild bitter residue at 100 ?g/mL had the potential in inhibitory ability against inflammation. These results in this study also indicated that extracts of wild bitter gourd IX residue activated PPAR? and suppressed the COX-2 protein expression. Furthermore, the human cytokine genes such as IL-1family and IL-3 expression were inhibition. Therefore, we suggest the possible mechanism is via activating the PPAR? signaling pathway and then suppress the NF-?B activation.
显示于类别:	[食品營養與保健生技學系] 博碩士論文

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