| 研究生: |
卓書齊 Cho, Shu Chi |
|---|---|
| 論文名稱: |
茶籽粕低皂素萃取物抑制脂多糖誘導的發炎及棕櫚酸誘導的胰島素阻抗 Tea seed meal saponin-reduced extract inhibits lipopolysaccharides-induced inflammation and palmitic acid-induced insulin resistance |
| 指導教授: |
蕭世裕
Shaw, Shyh‑Yu |
| 學位類別: |
博士 Doctor |
| 系所名稱: |
理學院 - 化學系 Department of Chemistry |
| 論文出版年: | 2024 |
| 畢業學年度: | 112 |
| 語文別: | 英文 |
| 論文頁數: | 108 |
| 中文關鍵詞: | 茶籽粕低皂素萃取物 、茶皂素 、抗發炎能力 、抗胰島素阻抗能力 |
| 外文關鍵詞: | TSMSRE, tea saponins, anti-inflammatory effect, anti-insulin resistance effect |
| 相關次數: | 點閱:102 下載:0 |
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茶籽粕為茶籽粹取油後所剩下的農業廢棄物。儘管茶籽粕含有豐富的天然化合物,但其高含量的茶皂素因具有毒性限制了其應用。因此,本研究旨在降低茶籽粕提取物中茶皂素的含量,並利用脂多糖 (lipopolysaccharides,LPS) 誘導發炎的 RAW 264.7 細胞模型以及利用棕櫚酸 (palmitic acid,PA) 誘導胰島素阻抗的 HepG2 細胞模型,探索茶籽粕低皂素萃取物(TSMSRE)的抗發炎潛力和抗胰島素阻抗潛力。
經皂素減少過程後,TSMSRE的茶皂素含量約為茶籽粕粗萃取物(TSMCE)的十分之一。更重要的是,TSMSRE在RAW 264.7細胞和HepG2細胞中的細胞毒性明顯低於TSMCE。進一步的分析顯示TSMSRE中存在的主要化合物為類黃酮 (flavonoid)。在抗發炎實驗中,TSMSRE作為強效的抑制抗發炎介質的抑制劑,在RAW 264.7細胞中顯著抑制了TNF-α、IL-1β、NO、PGE2、iNOS和COX-2的產生。此外,TSMSRE通過抑制RAW 264.7細胞中NF-κB和MAPK的細胞訊息傳遞路徑來發揮其抗發炎作用。在抗胰島素阻抗實驗中,TSMSRE通過顯著提高葡萄糖攝取及增強GLUT2、GLUT4和GSK-3β的表達,並抑制棕櫚酸引發的糖質新生 (Gluconeogenesis) 的高表現以達到抗胰島素阻抗的作用。此外,TSMSRE通過抑制HepG2細胞中MAPK的細胞訊息傳遞路徑,展現其抗胰島素阻抗效果。
總結來說,本研究結果表明TSMSRE能有效改善RAW 264.7細胞中脂多糖誘導的發炎反應和改善HepG2細胞中棕櫚酸誘導的胰島素阻抗。這些結果表明TSMSRE可做為一種有前景的抗發炎和抗胰島素阻抗的製劑。
Tea seed meal, derived from Camellia sinensis, possesses a richness of natural compounds. However, its considerable content of tea saponins raises concerns regarding cytotoxicity, posing a limitation on its utilization. Therefore, our study focused on reducing the tea saponin content in tea seed meal extract and exploring the anti-inflammatory potential of tea seed meal saponin-reduced extract (TSMSRE) using a lipopolysaccharide (LPS)-induced murine macrophage RAW 264.7 cell model and the anti-insulin resistance potential of TSMSRE using a palmitic acid-stimulated insulin resistance HepG2 cell model.
Following the saponin-reduction process, TSMSRE exhibited an approximately tenfold lower tea saponin content compared to that found in the tea seed meal crude extract (TSMCE). Importantly, TSMSRE displayed a significantly lower cytotoxicity compared to TSMCE in RAW 264.7 cells and HepG2 cells. Further analysis revealed the major compounds existed in TSMSRE were flavonoids. In the evaluation of its anti-inflammatory properties, TSMSRE exhibited as a potent suppressor of inflammatory mediators by markedly inhibiting the production of TNF-α, IL-1β, NO, PGE2, iNOS, and COX-2 in LPS-treated RAW 264.7 cells. Moreover, TSMSRE exerts its anti-inflammatory property by suppressing the activations of NF-κB and MAPK in RAW 264.7 cells. In the evaluation of its anti-insulin resistance properties, TSMSRE served as an anti-insulin resistance role by markedly improving glucose consumption, the expressions of GLUT 2, GLUT4, and GSK-3β and inhibiting the high expression gluconeogenesis in PA-activated HepG2 cells. In addition, TSMSRE exhibits its anti-insulin resistance effect by suppressing activation of MAPK in HepG2 cells.
In summary, our findings indicated that the anti-inflammatory potential of TSMSRE in ameliorating LPS-induced inflammatory responses in RAW 264.7 cells and the anti-insulin resistance potential of TSMSRE in ameliorating PA-induced insulin resistant in HepG2 cells. These results position TSMSRE as a promising agent for anti-inflammatory effect and anti-insulin resistance effect.
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校內:2027-04-30公開