两种新型硫酸化多糖(SPs),N10和K5从硫酸氨或硫酸钾中分离,浓度为10mM和5mM的牛樟芝液体培养物中,分别。N10和K5是半乳糖:葡萄糖摩尔比为约1:3的半乳糖葡聚糖。在脂多糖(LPS)刺激的RAW264.7细胞中,N10和K5表现出强烈的抗炎潜力,对IL-6和TNF-α产生的最大抑制为56%和23%,分别。机械分析显示N10和K5之间存在差异,N10抑制LPS刺激的RAW264.7细胞中ERK和p38的磷酸化。K5抑制LPS刺激的AKT和TGFβR-II的磷酸化。N10和K5被片段化为F1,F2和F3,其分子量分别为455、24、0.9和327、36、1.9kDa,分别。K5F2和K5F3表现出1:3和1:8的高硫酸化程度,从而产生强烈的抗炎作用,对IL-6和TNF-α产生的抑制作用最高,分别为83%和37%,分别。因此,低分子量和高硫酸化程度的SPs具有很强的抗炎活性。具体来说,K5F2抑制p38的磷酸化,K5F3抑制p38/JNK的信号通路。总的来说,结论SP的硫酸化程度影响抗炎反应。
Two novel sulfated polysaccharides (SPs), N10 and K5 were isolated from ammonium sulfate or potassium sulfate at concentrations of 10 mM and 5 mM in liquid cultures of Antrodia cinnamomea, respectively. N10 and K5 were galactoglucans with a galactose:glucose molar ratio of approximately 1:3. In lipopolysaccharide (LPS)-stimulated RAW264.7 cells, N10 and K5 exhibited strong anti-inflammatory potential, of 56 % and 23 % maximal inhibition of IL-6 and TNF-α production, respectively. Mechanical analysis revealed differences between N10 and K5, with N10 inhibiting the LPS-stimulated phosphorylation of ERK and p38 in RAW264.7 cells. K5 inhibited the LPS-stimulated phosphorylation of AKT and TGFβR-II. N10 and K5 were fragmented into F1, F2, and F3, the molecular weights of which were 455, 24, 0.9, and 327, 36, 1.9 kDa, respectively. K5 F2 and K5 F3 exhibited high degrees of sulfation of 1:3 and 1:8, resulting in strong anti-inflammation, of 83 % and 37 % highest inhibition of IL-6 and TNF-α production, respectively. Therefore, low-molecular-weight and high-sulfation-degree SPs exhibited strong anti-inflammatory activity. Specifically, K5 F2 inhibited the phosphorylation of p38, and K5 F3 suppressed the signaling pathway of p38/JNK. Overall, the sulfation degree of SPs is concluded to affect the anti-inflammatory responses.