文献类型：期刊文献

中文题名：当归多糖对肺癌微环境中骨髓间充质干细胞增殖及TAFs相关分子表达的影响

英文题名：Effects of Angelica sinensis Polysaccharide on Proliferation and Expression of Tumor-associated Fibroblasts Related Molecule of Bone Marrow Mesenchymal Stem Cells in the Lung Cancer Microenvironment

作者：武有明[1];张齐[1];刘永琦[1,2];何建新[1];伍志伟[1,2];高卓越[1];苏韫[1];骆亚莉[1];张利英[1];周妮娜[1]

第一作者：武有明

机构：[1]甘肃中医药大学甘肃省高校重大疾病分子医学与中医药防治研究省级重点实验室;[2]敦煌医学与转化省部共建教育部重点实验室

第一机构：甘肃中医药大学科研实验中心（甘肃省中医药标准化技术委员会秘书处）

年份：2015

卷号：37

期号：9

起止页码：1271

中文期刊名：中国细胞生物学学报

外文期刊名：Chinese Journal of Cell Biology

收录：CSTPCD;;CSCD:【CSCD2015_2016】；

基金：甘肃省杰出青年基金项目(批准号:1308RJDA008);国家自然科学基金(批准号:81360588)资助的课题~~

语种：中文

中文关键词：骨髓间充质干细胞;肿瘤微环境;当归多糖;肿瘤相关成纤维细胞

外文关键词：bone marrow mesenchymal stem cells; tumor microenvironment; Angelica sinensispolysaccharide; tumor associated fibroblasts

摘要：该文探讨了当归多糖(Angelica sinensis polysaccharide,ASP)对肺癌微环境中骨髓间充质干细胞(bone mesenchymal stem cells,BMSCs)增殖及肿瘤相关成纤维细胞(tumor-associated fi broblasts,TAFs)相关分子表达的影响。采用CCK-8法筛选ASP作用于BMSCs、肺癌Lewis(Lewis lung cancer,LLC)细胞的最佳有效浓度;利用Transwell小室建立BMSCs和LLC细胞的共培养体系并以ASP最佳浓度干预共培养体系,分为BMSCs组、LLC组、BMSCs与LLC共培养组(Co-BMSCs组)和ASP-Co-BMSCs组;通过倒置相差显微镜观察细胞的形态,生长曲线检测细胞的增殖能力,流式细胞术检测各组细胞周期,Western blot技术检测各组BMSCs TAFs标记分子α-SMA、FAP蛋白质的表达。结果显示,与对照组相比,ASP 50μg/m L促进BMSCs细胞增殖(P<0.01),而对LLC细胞增殖则有明显抑制作用(P<0.01);与BMSCs组相比,Co-BMSCs组细胞生长速度显著增加(P<0.01),Co-BMSCs组细胞G0/G1期比例降低,S期比例升高,差异有统计学意义(P<0.05);与Co-BMSCs组相比,ASP-Co-BMSCs组G0/G1期比例升高,S期比例降低,差异有统计学意义(P<0.05);蛋白印迹结果表明,与BMSCs组相比,Co-BMSCs组α-SMA、FAP蛋白质表达均明显升高,差异有统计学意义(P<0.01);与Co-BMSCs组相比,ASP-Co-BMSCs组α-SMA、FAP蛋白质表达均下降(P<0.01)。结果表明,当归多糖可抑制肺癌LLC共培养微环境中BMSCs的异常增殖及TAFs相关分子表达。
This work was aimed at investigating effects of Angelica sinensis polysaccharide （ASP） on proliferation and expression of TAFs related molecules of bone marrow mesenchymal stem cells （BMSCs） in the lungcancer microenvironment. The optimal concentration of ASP on the effect of Lewis lung cancer （LLC） and BMSCs was selected by CCK-8. After establishing the co-culture system of LLC and BMSCs by transwell chambers, we intervened it by the effective concentration of ASP. The study contained BMSCs, LLC, Co-BMSCs and ASP-Co-BMSCs group. The morphology of cells was observed by phase-contrast microscopy. The proliferation capability of cells was tested by CCK-8. The cell cycle was tested by flow cytometry. The protein expressions of biomarkers of TAFs-a-SMA and FAP of each group was detected by Western blot. Our results indicated that ASP （50 μg/mL） promoted BMSCs proliferation while had an obvious inhibitory effect on LLC proliferation （P〈0.01）. Compared with BMSCs group, the growth rate of Co-BMSCs increased significantly （P〈0.01）, the ratio of cells in GdG1 phase of Co-BMSCs group was reduced with an increase in S phase （P〈0.05）. Compared with Co-BMSCs group, the proportion of cells in G0/G1 phase of ASP-Co- BMSCs group was increased, and the proportion of cells in S phase was significantly decreased （P〈0.05）. In the results of Western blot, the protein expression of α-SMA and FAP in Co-BMSCs group raised obviously compared with that in BMSCs group （P〈0.01）. Compared with Co-BMSCs group, the expression of α-SMA and FAP protein decreased in the group of Co-BMSCs intervened with ASP （P〈0.01）. Our results suggested that ASP could inhibit the proliferation of BMSCs in lewis lung cancer microenvironment and expression of TAFs related molecule.