以髓源抑制性细胞为靶点的竹荪多糖抗肿瘤机制研究  

Antitumor mechanism of polysaccharide from dictyophora targetedon myeloid derived suppressor sell

作　　者：江洪[1] 王小红[2] JIANG Hong;WANG Xiaohong(Hangzhou First People's Hospital,Hangzhou 310006,China;Zhejiang Cancer Hospital,Hangzhou 310022,China)

机构地区：[1]杭州市第一人民医院,浙江杭州310006 [2]浙江省肿瘤医院,浙江杭州310022

出　　处：《中国医药科学》2019年第24期21-26,共6页China Medicine And Pharmacy

基　　金：浙江省杭州市科技发展计划项目(20140633B02)

摘　　要：目的研究竹荪多糖诱导髓源抑制性细胞(MDSC)凋亡的效应及分子机制。方法构建荷瘤小鼠模型,检测竹荪多糖的体内抗肿瘤活性,体外实验中通过流式细胞学检测竹荪多糖对MDSC比例及亚群的影响,采用Western Blot检测竹荪多糖处理后MDSCs分子变化。结果竹荪多糖DP15可抑制小鼠体内路易斯肺癌细胞系LLC的肿瘤生长;DP15可显著下调荷瘤小鼠脾脏中MDSCs比例,该效应与上调MDSCs中P53基因及下调Bcl-2基因表达有关。结论竹荪多糖DP15通过促进MDSC凋亡而下调其比例,DP15可作为候选的抗肿瘤生物活性分子。Objective To study the effect of Polysaccharide from Dictyophora on apoptosis of myeloid derived suppressor cell(MDSC)and its molecular mechanism.Methods The tumor bearing mice model was established and the antitumor activity in vivo was detected.The effect of Polysaccharide on the proportion and subsets of MDSCs was detected byflow cytometry in vitro.The molecular changes of MDSCs were detected by Western blot.Results DP15 could inhibit the tumor growth of Lewis lung cancer cell line LLC in mice,and significantly reduce the MDSCs proportion in spleen of tumor bearing mice,which was related to the up-regulation of P53 gene and down-regulation of Bcl-2 gene expression in MDSCs.Conclusion DP15 can reduce the proportion of MDSC by promoting the apoptosis of MDSC and can be used as a candidate antitumor bioactive molecule.

关 键 词：竹荪 多糖 髓源抑制性细胞 抗肿瘤 

分 类 号：R285[医药卫生—中药学]