Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/92629
標題: 龍眼核萃取物抗發炎作用之研究
Anti-inflammatory Activities of Longan seed Extract
作者: 鍾雪玉
Hsueh-Yu Chung
關鍵字: 龍眼核;抗發炎;λ角叉菜膠;前列腺素E2;一氧化氮;絲裂原活化蛋白激?;環氧化?;誘導型一氧化氮合成?;凋亡蛋白?;Longan seed;Anti-Inflammation;λ-carrageenan;PGE2;NO;MAPKs;COX-2;iNOS;Caspase-3
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摘要: 
龍眼核(Longan seed; LS)雖已有長時間的使用經驗,用於割、燒燙傷口的疼痛及感染,能定疼止血,然而缺乏足夠直接的科學證據。我們以脂多醣(Lipopolysaccharides; LPS)誘發BV-2微小膠細胞in vitro,以LPS/λ角叉菜膠(λ- carrageenan)誘導 SD大鼠(Sprague-Dawley)發炎in vivo,探討龍眼核萃取物之抗發炎活性及細胞分子作用機制。
In vitro,研究結果顯示,龍眼核萃取物可降低LPS誘導BV-2細胞的一氧化氮(NO)、介白素1(interleukin-1beta; IL-1?)、介白素6(interleukin-6; IL-6)和前列腺素E2(prostaglandin E2; PGE2)生成量(釋放量)。Western blotting,發現藉由dose-dependently 抑制JNK(c-Jun NH2-terminalprotein kinase)表現。以及ERKs(Extracellular signal-regulated kinases)、凋亡蛋白?(Caspase-3)和環氧?2(cyclooxygenase; COX-2)的蛋白質表現亦被抑制。In vivo,在LPS/λ- carrageenan誘導的發炎模式中,龍眼核萃取物降低LPS誘導的SD大鼠血中IL-1? 、IL-6 和COX-2生成量(釋放量),及降低λ- carrageenan誘導的SD大鼠蹠蹼組織液中NO 、IL-1? 、IL-6 和PGE2生成量(釋放量)。藉由抑制促發炎細胞激素IL-1? 、IL-6 和PGE2生成及JNK 和COX-2的表現以達到抗發炎作用的保護機制。

Longan seed (LS) has been traditionally used for the treatment of wounded pain of cut, burn, and infection; however, the direct evidence is lacking. We investigated the anti- inflammation effect of LS extract (LSE) on lipopolysaccharide (LPS) induced inflammation of BV-2 microglial cells in vitro and LPS/λ-Carrageenan (CARR)-induced inflammation or paw edema of Sprague-Dawley (SD) rats in vivo.
Our results showed that LSE decreased LPS-induced nitric oxide (NO), interleukin -1? (IL-1?), IL-6, and prostaglandin E2 (PGE2) production of BV-2 cells in vivo. LSE dose-dependently inhibited LPS-induced JNK (c-Jun NH2-terminalprotein kinase)of BV-2 cells and decreased ERKs (Extracellular signal-regulated kinases), Caspase-3, cyclooxygenase (COX-2) expressions.LSE not only decreased IL-1?, IL-6, and COX-2 production of blood in LPS-treated rats but also decreased NO, IL-1?, IL-6, and PGE2 production in paw edema by λ- carrageenan induced in vivo.These results indicate that the protective mechanism of LSE involves an anti-inflammation effect through inhibition of proinflammatory cytokines (IL-1?, IL-6, and PGE2), JNK, and COX-2 expressions .
URI: http://hdl.handle.net/11455/92629
其他識別: U0005-2811201416191016
Rights: 不同意授權瀏覽/列印電子全文服務
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