摘要: | 喪黃(Phellinus linteus)自古以來即為一種著名的名貴菇類藥材,也是一種具有高經濟效益的保健食品材料。民間多認為桑黃具有抗發炎、保肝及免疫調節等功效。動物實驗结果發現自液態培養之桑黃菌絲體所分離的多醣具有免疫調節及抗癌(肺及黑色素癌)活性。然而,有關固態培養桑黃之體外免疫調節特性及其免疫訊息路徑與分子作用機制目前尚不清楚,因此值得深入研究。本研究主要目的為桑黃子實體之萃取物(水及 95 % 酒精)及多醣對脂多醣 (LPS) 誘導人類單核細胞 (THP-1) 之細胞存活率及免疫分子訊息傳導如訊息分子[TLR-4及MyD88]系統、細胞激素 (TNF-α, IL-1α, IL-1β, IL-4)、一氧化氮 (NO) 生成量及血管黏附分子-1 (VCAM-1) 分泌之影響。 MTT 分析结果顯示自桑黃分離之多醣 (PLP) 對LPS 誘導 THP-1細胞之細胞存活率表現比其他萃取物為佳。 PLP 在濃度 1.0 - 5.0 μg/ml 下具有抗 LPS 誘導細胞死亡,且呈劑量型保護效應。 PLP 在濃度 1.0 - 5.0 μg/ml 下具有抑制一氧化氮的生成。 PLP在 5.0 μg/ml 可顯著地抑制 LPS 所誘導之 TLR-4 、細胞激素 ( TNF-α, IL-1α, IL-1β 及 IL-4) 及血管黏附分子-1 (VCAM-1) 表現。這些结果證實 PLP 具有明顯地免疫調節特性,其作用機制係透過抑制 LPS 誘導一氧化氮、細胞激素 (TNF-α, IL-1α, IL-1β 及 IL-4) 、血管黏附分子-1 (VCAM-1)之釋放及 MyD88 訊息路徑。 Phellinus linteus (PL), a medicinal fungus, has long been considered as a high value ingredient for traditional Chinese medicine and for health food development. It is generally believed to possess anti-inflammatory, hepatoprotective, immunomodulatory and other therapeutic properties. Animal studies showed that polysaccharides from liquid cultured P. linteus mycelia possessed immunomodulatory and anti-cancer (lung cancer and melanoma) activities. However, the immunomodulatory properties and molecular mechanism (s) of action of different PL extracts (aqeous;WPL;ethanolic EPL) and polysaccharides (PLP) from P. linteus remain unknown. The aim of this study was to examine the effects of P. linteus polysaccharides (PLP) on cell viability, nitric oxide (NO) and molecular signaling cascades, such as signaling molecules [TLR(-4) and MyD88], cytokines (TNF-α, IL-1α, IL-1β and IL-4), TRAF-6 and vascular adhesion molecular-1 (VCAM-1) secretion in LPS-induced human monocytic cells (THP-1). At concentrations 1.0-5.0 μg/ml, PLP dose-dependently protected against LPS-induced cell death. At concentrations 1.0-5.0 μg/ml, PLP dose-dependently inhibitor nitric oxide secretion. At 5.0 μg/ml, PLP significantly blocked the LPS induction of cytokines (TNF-α, IL-1α, IL-1β and IL-4), and vascular adhesion molecular-1 (VCAM-1) expression, but has no effect on TLR-4. These results demonstrate that PLP possessed potent immuno-regulatory property, and its mechanism of action could be through the inhibition of LPS-induced release of cytokines (TNF-α, IL-1α, IL-1β and IL-4), VCAM-1 expression and MyD88 signaling pathway. |