Kim Gi-Young, Roh Su-In, Park Soon-Kew, Ahn Soon-Cheol, Oh Yang-Hyo, Lee Jae-Dong, Park Yeong-Min
Department of Microbiology, College of Natural Sciences, Pusan National University, South Korea.
Biol Pharm Bull. 2003 Oct;26(10):1418-23. doi: 10.1248/bpb.26.1418.
This study reports that acidic polysaccharide (PL) isolated from Phellinus linteus alleviated the septic shock induced by high dose lipopolysaccharide (LPS) injection in mice. To examine the origin of this effect, we investigated cytokine production in serum and the expression of MHC II in B cells and macrophages in areas of inflammation. Pretreatment with PL 24 h before LPS administration resulted in a significant inhibition of up to 68% of circulating tumor necrosis factor (TNF)-alpha, a moderate reduction of 45% of interleukine (IL)-12 and 23% of IL-1beta, but no significant reduction in IL-6. In addition, the expression of MHC II in B cells and macrophages was examined. Our results show that LPS-stimulated cytokine release and the level of MHC II can be modulated by in vivo administration of soluble PL in mice. The decrease of IL-1beta, IL-12 and TNF-alpha in sera and the down-modulation of MHC II during septic shock may contribute to the long survival of mice by PL. Administration of PL in vivo decreases IL-2, IFN-gamma and TNF-alpha production in splencotyes and enhances spontaneous cell apoptosis in macrophages and lymphocytes stimulated with LPS in vitro. Thus, part of the anti-inflammatory effects of PL treatment in vivo may result from the enhanced apoptosis of a portion of the activated macrophages and lymphocytes. The ability of PL to significantly reduce the TNF-alpha production indicates the potential of the polysaccharides in possible therapeutic strategies that are based on down-regulation of TNF-alpha.
本研究报告称，从桑黄中分离出的酸性多糖（PL）可减轻高剂量脂多糖（LPS）注射诱导的小鼠脓毒症休克。为了探究这种作用的来源，我们研究了血清中细胞因子的产生以及炎症区域B细胞和巨噬细胞中MHC II的表达。在给予LPS前24小时用PL预处理可显著抑制循环肿瘤坏死因子（TNF）-α高达68%，适度降低白细胞介素（IL）-12 45%和IL-1β 23%，但IL-6无显著降低。此外，还检测了B细胞和巨噬细胞中MHC II的表达。我们的结果表明，体内给予可溶性PL可调节LPS刺激的细胞因子释放和MHC II水平。脓毒症休克期间血清中IL-1β、IL-12和TNF-α的降低以及MHC II的下调可能有助于PL使小鼠长期存活。体内给予PL可降低脾细胞中IL-2、IFN-γ和TNF-α的产生，并增强体外LPS刺激的巨噬细胞和淋巴细胞的自发细胞凋亡。因此，PL体内治疗的部分抗炎作用可能源于部分活化巨噬细胞和淋巴细胞凋亡的增强。PL显著降低TNF-α产生的能力表明该多糖在基于下调TNF-α的可能治疗策略中的潜力。
