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黄芪多糖对炎性微环境中BMSCs的IL-6R、TNFR及肿瘤相关基因表达的影响     被引量:7

Effects of Astragalus Polysaccharides on Expression of IL-6R, TNFR and Tumor Related Genes of Bone Marrow Mesenchymal Stem Cells in Inflammatory Microenvironment

文献类型:期刊文献

中文题名:黄芪多糖对炎性微环境中BMSCs的IL-6R、TNFR及肿瘤相关基因表达的影响

英文题名:Effects of Astragalus Polysaccharides on Expression of IL-6R, TNFR and Tumor Related Genes of Bone Marrow Mesenchymal Stem Cells in Inflammatory Microenvironment

作者:骆亚莉[1,2,3];张利英[2,3];李程豪[2];张艳辉[2];刘永琦[2];安方玉[2,3];冯彩琴[2];李研[2]

第一作者:骆亚莉

机构:[1]甘肃中医药大学,基础医学院病理教研室,兰州730000;[2]甘肃中医药大学,重大疾病分子医学与中医药防治研究重点实验室,兰州730000;[3]甘肃中医药大学,敦煌医学与转化教育部重点实验室,兰州730000

第一机构:甘肃中医药大学基础医学院(敦煌医学研究所)

年份:2018

卷号:40

期号:11

起止页码:1819

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:【CSCD2017_2018】;

基金:国家自然科学基金(批准号:81760804、81360588)资助的课题~~

语种:中文

中文关键词:黄芪多糖;IL-6;TNF-α;炎性微环境;骨髓间充质干细胞;IL-6R;TNFR

外文关键词:astragalus polysaccharide;IL-6;TNF-alpha;inflammatory microenvironment;BMSCs;IL-6R;TNFR

摘要:该文旨在观察黄芪多糖(astragalus polysaccharide, APS)对IL-6和TNF-α所致炎性微环境中骨髓间充质干细胞(bone mesenchymal stem cells, BMSCs)白介素-6受体(IL-6 receptor, IL-6R)、肿瘤坏死因子受体(tumor necrosis factor receptor, TNFR)表达的影响,探讨IL-6和TNF-α导致BMSCs炎性损伤的可能物质基础。首先运用100 ng/mL IL-6和50 ng/mL TNF-α建立炎性微环境。设立对照组(control组)、模型组(D组)和50μg/m L黄芪多糖干预组(H组)。之后,应用ELISA法检测s IL-6R的表达水平。免疫荧光法检测IL-6R、gp130、TNFR I、TNFR II的表达水平。Western blot技术检测抑癌基因P53、PTEN和原癌基因Ras、C-myc的蛋白表达水平。检测结果显示,与对照组比较,模型组细胞上清液中的s IL-6R含量降低,模型组细胞IL-6R、gp130、TNFR I、TNFR II、Ras、C-myc表达均升高, P53、PTEN表达均降低。与模型组比较,黄芪多糖组细胞上清液sIL-6R含量升高,细胞IL-6R、gp130、TNFR I、TNFR II、Ras、C-myc表达均下降,而P53、PTEN表达均升高。结果提示,黄芪多糖能够减弱炎性微环境对刺激BMSCs表达IL-6R、TNFR的影响作用,并且维护肿瘤相关基因表达的相对稳定性。
The purpose of this study is to observe the expression of IL-6 R and TNFR of bone marrow mesenchymal stem cells in inflammatory microenvironment induced by IL-6 and TNF-α, and to investigate the effect of astragalus polysaccharide on IL-6 R and TNFR expression in order to explore the possible mechanism of IL-6 and TNF-α on inflammatory injury of BMSCs. The inflammatory microenvironment was established by using 100 ng/mL IL-6 and 50 ng/mL TNF-α. BMSCs were divided into control group, model group(D group) and 50 μg/mL APS intervention group(H group). The expression level of sIL-6 R in the supernatant was determined by ELISA. The levels of IL-6 R, GP-130, TNFR I and TNFR II were detected by immunofluorescence methods. Western blot was used to detect the expression level of P53, PTEN and Ras and C-myc. Results showed that compared with the control group, the content of sIL-6 R in the supernatant decreased, and the levels of IL-6 R, GP 130, TNFR I and TNFR II increased in model group. Compared with the model group, the interposition of APS increased the content of sIL-6 R and decreased the expression of IL-6 R, GP 130, TNFR I and TNFR II. Compared with the control group, the expression of Ras, C-myc protein increased and that of P53 and PTEN decreased in model group. After the intervention of APS, the expression of Ras, C-myc protein decreased, while P53 and PTEN protein increased. Collectively, the present study demonstrates that APS could not only decrease the influence of BMSCs on IL-6 R and TNFR in inflammatory microenvironment, but also maintain the expression level of tumor related genes stability.

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