软骨多糖诱导小鼠S180细胞凋亡的作用机制

目的研究软骨多糖对S180荷瘤小鼠的作用,并探讨其抑瘤作用机制。方法采用小鼠肉瘤S180细胞建立动物腹水瘤模型,通过腹腔注射软骨多糖进行治疗,治疗期间抽取腹水瘤细胞进行细胞生物学分析。通过HE染色,流式细胞术、TUNEL法检测细胞形态学方面、细胞周期及凋亡率的变化情况;通过免疫荧光方法检测Fas、增殖细胞核抗原(PCNA)的表达情况。结果软骨多糖可以明显提高S180荷瘤小鼠的生存率,细胞形态学观察可见细胞出现细胞质浓缩、核固缩及凋亡小体等现象。软骨多糖作用后的S180细胞,其细胞周期被阻遏于G2/M期,Fas蛋白的表达水平于给药24 h后升高,增殖细胞核抗原PCNA表达下降。结论软骨多糖可能通过影响肿瘤细胞周期和Fas、PCNA蛋白的表达来诱导S180细胞凋亡,并显著抑制肿瘤细胞的生长,延长S180荷瘤小鼠的生存时间,研究证实动物软骨多糖具有潜在的药用价值。

Effect of Cartilage Polysaccharide and Its Mechanism to Induce Apoptosis in Mouse S180 Cells

Objective To study the effect of cartilage polysaccharide on S_(180)-bearing mice and its anti-tumor mechanism.Methods The S_(180)-bearing mouse model was prepared and treated by i.p.injection of cartilage polysaccharide.The tumor cells morphology was examined by light microscopy.The cell cycle was analyzed by flow cytometry,and apoptotic rate was determined by TUNEL assay.The expression of Fas and PCNA proteins was studied by immunofluorescent staining.Results The survival rate of S_(180)-bearing mice was significantly increased by cartilage polysaccharide treatment in comparison with that of control group.Cell shrinkage,nuclear condensation and apoptotic bodies were detected by morphological observation.The cell cycle of S_(180) cells was arrested at G_2/M phase. The expression of Fas protein was increased and PCNA expression was decreased at 24 h after cartilage polysaccharide treatment.Conclusion Cartilage polysaccharide induces apoptosis of S_(180) cells by cell cycle arrest and influences the expression of Fas and PCNA proteins,and inhibits tumor cell growth,and prolong survival time of S_(180)-bearing mice.Those findings indicate that cartilage polysaccharide might become a novel anti-tumor agent in future.