Isolation conditions immunomodulatory and anti-inflammatory activites of rice bran feruloylated oligosaccharides

• Main Authors: Yi-Ting Fang, 方怡婷
• Other Authors: Hua-Han Chen
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/78511314853398292418

碩士 === 中華醫事科技大學 === 生物科技研究所 === 96 === This study was to investigate the optimization conditions of feruloylated oligosaccharides preparation from rice bran by acid hydrolysis and to evaluate the immunomodulatory function of feruloylated oligosaccharides. To obtain the optimization conditions of feruloylated oligosaccharides preparation, response surface methodology (RSM) was introduced in this study. The optimal condition of 193 mM of TFA and 1.36 h of hydrolysis time was derived from canonical analysis. 2.2% of feruloylated oligosaccharides recovery was verified from predicted optimal condition and confirmed the fitness and applicability of this model. The immunomodulatory activity of feruloylated oligosaccharides was evaluated through RAW264.7 macrophage cells model. Inflammatory mediators, including the nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and prostaglandins E2 (PGE2) were surveyed separately. The results showed that the increasing of NO releasing and TNF-α, IL-1β, IL-6 and PGE2 secretion were in proportion to the increasing concentrations of feruloylated oligosaccharides. Furthermore, inflammation-prevent model (Model A) and inflammation-repairing model (Model B) of feruloylated oligosaccharides were both investigated to clarify anti-inflammatory activity in the LPS-induced RAW264.7 macrophage cells model. The data from model A and model B revealed that feruloylated oligosaccharides could significantly reduce the LPS-induced NO secretion and increased IL-10 production, but inhibited pro-inflammatory cytokine and PGE2 production. Therefore, feruloylated oligosaccharides could reveal the immunomodulatory activity. In addition, it also had the inflammation-prevent and inflammation-repair abilities against LPS-induced inflammatory effect.