目的研究水溶性壳聚糖(water soluble chitosan,WSC)对脂多糖诱导的小鼠腹腔巨噬细胞凋亡的影响,并探讨其机制。方法无菌分离小鼠腹腔巨噬细胞,分为脂多糖刺激组、WSC与脂多糖共同作用组,并设磷酸盐缓冲液空白对照组,培养24 h后,流式细胞术检测细胞凋亡情况和活化胱天蛋白酶(caspase)-3的表达,Griess法测定一氧化氮释放量。结果各组细胞培养24 h后,与磷酸盐缓冲液空白对照组相比,脂多糖刺激组细胞的凋亡明显增加,一氧化氮的释放和caspase-3的活化明显增强;WSC与脂多糖共同作用组凋亡的巨噬细胞较脂多糖刺激组明显减少,一氧化氮的释放和caspase-3的活化也受到了明显的抑制。结论 WSC通过抑制一氧化氮的释放和caspase-3的活化阻止脂多糖诱导的巨噬细胞凋亡。 Objective To investigate the effect of water-soluble chitosan (WSC) on lipopolysaccharide-induced apoptosis of murine peritoneal macrophages and its mechanism. Methods Mouse peritoneal macrophages were isolated aseptically and divided into three groups: lipopolysaccharide stimulation group, WSC group and lipopolysaccharide group, and a phosphate buffer control group. After cultured for 24 h, the apoptosis of cells was detected by flow cytometry And activation of caspase-3 expression, Griess method for the determination of nitric oxide release. Results Compared with phosphate buffer control group, the apoptosis of cells in LPS group was significantly increased, the release of nitric oxide and the activation of caspase-3 were significantly increased after 24 h incubation in each group. WSC and lipopolysaccharide were Apoptotic macrophages in the treatment group were significantly reduced compared with those in the LPS group, and the release of nitric oxide and the activation of caspase-3 were also significantly inhibited. Conclusion WSC prevents lipopolysaccharide-induced apoptosis of macrophages by inhibiting the release of nitric oxide and the activation of caspase-3.