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目的 :观察当归多糖对小鼠腹腔巨噬细胞产生细胞毒效应分子的影响。方法 :从BALB/c小鼠的腹腔分离巨噬细胞 ,并进行原代细胞培养。采用MTT比色法及紫外分光光度法 ,检测当归多糖对腹腔巨噬细胞释放一氧化氮 (NO)、肿瘤坏死因子α(TNF α)、活性氧 (ROS)以及诱导型一氧化氮合酶 (iNOS)和溶菌酶 (LSZ)活性的影响。结果 :当归多糖可激活巨噬细胞释放NO、TNF α和ROS等效应分子 ,并显著提高LSZ的活性。当归多糖可能通过提高巨噬细胞iNOS的活性而增加NO的释放量 ,但其与脂多糖 (LPS)无协同促进NO释放的作用。当归多糖体外无直接杀伤肿瘤细胞的作用 ,但其与巨噬细胞共孵育的培养上清具有杀伤L92 9细胞的作用。结论 :当归多糖可促进巨噬细胞释放NO、TNF α及ROS等细胞效应分子 ,并可通过作用于巨噬细胞而促进TNF α的分泌 ,发挥间接的抗肿瘤免疫作用
Objective : To observe the effect of angelica polysaccharides on the production of cytotoxic effector molecules in mouse peritoneal macrophages. METHODS: Macrophages were isolated from the abdominal cavity of BALB/c mice and primary cell cultures were performed. MTT colorimetric assay and ultraviolet spectrophotometry were used to detect the release of nitric oxide (NO), tumor necrosis factor α (TNF α), reactive oxygen species (ROS) and inducible nitric oxide synthase from peritoneal macrophages. Effects of iNOS) and lysozyme (LSZ) activity. RESULTS: Angelica polysaccharide could activate macrophages to release NO, TNF α and ROS and other effector molecules, and significantly increase the activity of LSZ. Angelica polysaccharide may increase the release of NO by increasing the activity of iNOS in macrophages, but it does not synergistically promote the release of NO with lipopolysaccharide (LPS). Angelica polysaccharide did not directly kill tumor cells in vitro, but its culture supernatant co-incubated with macrophages had the effect of killing L92 9 cells. Conclusion : Angelica polysaccharides can promote the release of NO, TNF α and ROS from macrophages, and promote the secretion of TNF α by acting on macrophages to exert indirect anti-tumor immunity.