Effects of the wild bitter gourd and white bitter gourd extracts on the inflammatory responses of LPS-induced murine Raw 264.7 macrophages

• Main Authors: Wen-Tzu, 雲文姿
• Other Authors: Chong-Kuei Lii
• Format: Others
• Language: zh-TW
• Published: 2005
• Online Access: http://ndltd.ncl.edu.tw/handle/25757238956190909988

碩士 === 中山醫學大學 === 營養學研究所 === 93 === Recent clinic research shows the etiology of cardiovascular diseases is associated with the chronic inflammation. This evidence implicates that decrease of chronic inflammation may help to maintain normal cardiovascular function. This study was designed to investigate the biological activity of wild bitter gourd and white bitter gourd extracts on NO, PGE2, and IL-1β production in LPS-stimulated RAW 264.7 macrophages. Result indicates the hot water (0.5-2mg/ml) and 95% ethanol (25-50μg/ml) extracts of the wild bitter gourd are effectively inhibit NO production (p<0.05). At 50μg/ml, a 36% decrease of NO production was noted on ethanol extract-treated cells as compared to the cells treated with LPS alone. In addition, a 37% suppression of PGE2 secretion was also noted by 50μg/ml ethanol extract. As compared to the effect of the wild bitter gourd, extracts from the white bitter gourd showed a much less inhibition on NO and PGE2. Western blot analysis revealed that iNOS and pro-IL-1β levels were dose-dependently decreased in the hot water- and ethanol-extracts of the wild bitter gourd. However, the suppression of COX2 expression was noted only in cells treated with the ethanol extract. Electrophoresis mobility shift assay further showed both wild bitter gourd hot water- and ethanol extracts inhibit NF-κB activation. The phenolic compound contents of each wild bitter gourd extract was in an order of ethanol (31.82±4.91mg/g)>ethyl acetate (17.55±3.58mg/g)>hot water (11.15±1.16mg/g)>cold water (8.53±0.15mg/g). These results suggest the ethanol-extract of wild bitter gourd is effectiveness on the inhibition of LPS-induced iNOS and pro-IL-1β protein expression and NO and PGE2 production. The possible mechanism is probably related to its inhibition on the NF-κB activation.