大分子灵芝多糖对非小细胞肺癌细胞增殖、迁移和侵袭能力的抑制作用
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摘要
目的:探讨超滤管截留得到的大分子量灵芝多糖(ultrafiltered macromolecular Ganoderma lucidum polysaccharide,UM-GLP)对非小细胞肺癌细胞增殖、迁移和侵袭能力的抑制作用。方法:以非小细胞肺癌细胞A549和NCI-H1299作为研究对象,并以空白培养基和紫杉醇(PTX)处理分别作为空白对照和阳性对照。采用MTT法检测UM-GLP对A549和NCI-H1299细胞增殖的抑制作用,划痕实验检测UM-GLP对A549和NCIH1299细胞迁移能力的抑制作用,Transwell实验检测UM-GLP对A549和NCI-H1299细胞侵袭能力的抑制作用。结果:MTT实验结果显示,随着UM-GLP和PTX药物浓度的增加,细胞增殖抑制率明显增加,UM-GLP浓度在0.5~2.0 mg/ml时,与PTX浓度在25~100 nmol/L的抑制效果相仿。A549和NCI-H1299细胞划痕实验结果显示,与空白对照组比较,UM-GLP组和PTX组的迁移距离均明显缩短(P<0.05)。Transwell实验结果显示,UM-GLP(2 mg/ml)处理后,非小细胞肺癌细胞侵袭数量显著低于空白对照组(P<0.05);并且UM-GLP对A549细胞侵袭能力的抑制作用与紫杉醇组(0.1μmol/L)相当,对NCI-H1299细胞侵袭能力的抑制作用小于紫杉醇组(0.1μmol/L)(P<0.05)。结论:大分子量灵芝多糖可有效抑制非小细胞肺癌细胞A549和NCI-H1299的增殖、迁移和侵袭能力。
Objective: To investigate the inhibitory effects of ultrafiltered macromolecular Ganoderma lucidum polysaccharide( UMGLP) on the proliferation,migration and invasion of non-small cell lung cancer cells( NSCLC). Methods: The non-small cell lung cancer cell lines A549 and NCI-H1299 were used as the study subjects. Blank culture medium and paclitaxel( PTX) treatment were used as the blank control and positive control,respectively. The inhibitory effect of UM-GLP on the proliferation of A549 cells and NCI-H1299 cells was examined by MTT assay. The inhibitory effect of UM-GLP on the migration of A549 cells and NCI-H1299 cells was detected by scratch test. The inhibitory effect of UM-GLP on the invasion of A549 cells and NCI-H1299 cells was evaluated by Transwell assay.Results: The MTT results showed that,with the increase of UM-GLP and PTX concentration,the inhibition rate of cell proliferation was increased significantly. When the concentration of UM-GLP was at 0.5-2.0 mg/ml,the inhibition effect was similar to that of PTX at 25-100 nmol/L. In the scratch test,compared with the blank control group,the cell migration distances of A549 cells and NCI-H1299 cells were significantly shortened in the UM-GLP group and PTX group( P<0.05). Transwell assay indicated that after treatment with UM-GLP( 2 mg/ml),the number of invaded NSCLC was significantly less than that in the blank control group( P<0.05),the inhibitory effect of UM-GLP on A549 cell invasion was comparable to that of the paclitaxel( 0.1 μmol/L),and the inhibitory effect of UM-GLP on NCI-H1299 cell invasion was weaker than that of paclitaxel( 0.1 μmol/L)( P<0.05). Conclusion: UM-GLP can effectively inhibit the proliferation,migration and invasion of NSCLC A549 cells and NCI-H1299 cells.
Objective: To investigate the inhibitory effects of ultrafiltered macromolecular Ganoderma lucidum polysaccharide( UMGLP) on the proliferation,migration and invasion of non-small cell lung cancer cells( NSCLC). Methods: The non-small cell lung cancer cell lines A549 and NCI-H1299 were used as the study subjects. Blank culture medium and paclitaxel( PTX) treatment were used as the blank control and positive control,respectively. The inhibitory effect of UM-GLP on the proliferation of A549 cells and NCI-H1299 cells was examined by MTT assay. The inhibitory effect of UM-GLP on the migration of A549 cells and NCI-H1299 cells was detected by scratch test. The inhibitory effect of UM-GLP on the invasion of A549 cells and NCI-H1299 cells was evaluated by Transwell assay.Results: The MTT results showed that,with the increase of UM-GLP and PTX concentration,the inhibition rate of cell proliferation was increased significantly. When the concentration of UM-GLP was at 0.5-2.0 mg/ml,the inhibition effect was similar to that of PTX at 25-100 nmol/L. In the scratch test,compared with the blank control group,the cell migration distances of A549 cells and NCI-H1299 cells were significantly shortened in the UM-GLP group and PTX group( P<0.05). Transwell assay indicated that after treatment with UM-GLP( 2 mg/ml),the number of invaded NSCLC was significantly less than that in the blank control group( P<0.05),the inhibitory effect of UM-GLP on A549 cell invasion was comparable to that of the paclitaxel( 0.1 μmol/L),and the inhibitory effect of UM-GLP on NCI-H1299 cell invasion was weaker than that of paclitaxel( 0.1 μmol/L)( P<0.05). Conclusion: UM-GLP can effectively inhibit the proliferation,migration and invasion of NSCLC A549 cells and NCI-H1299 cells.
引文
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[14]王洁茹,王金英,张婷婷,等.黄芪多糖调节黑色素瘤小鼠PD-1/PD-Ls分子表达的研究[J].上海中医药大学学报,2014,25(5):74-79.
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[17]熊川,罗强,金鑫,等.人工栽培灵芝中多糖的部分理化性质及免疫调节作用[J].微生物学通报,2018,45(4):825-835.
[18]陈源红,邹佳峻,李松波.灵芝多糖对人肝癌细胞Hep G2增殖及体外迁移的影响[J].广东医学,2018,39(11):1625-1628.
[19]梁曾恩妮.灵芝多糖对结肠癌细胞增殖抑制和凋亡的影响初步研究[D].长沙:湖南农业大学,2014.
[2]XU Y,ZHANG Y,WANG Z,et al. The role of serum angiopoietin-2 levels in progression and prognosis of lung cancer[J]. Medicine,2017,96(37):e8063.
[3]胡毅,陶海涛.晚期非小细胞肺癌的药物治疗进展[J].中国药物应用与监测,2014,11(6):329-332.
[4]朱洪源,陈成.晚期非小细胞肺癌的药物治疗进展[J].中国现代医学杂志,2011,21(33):4154-4157.
[5]张朋,刘苓霜.中医药调节肺癌免疫机制研究进展[J].上海中医药大学学报,2015,29(5):102-106.
[6]李斯文,石颖,李晓林,等.肿瘤康胶囊辅助治疗非小细胞肺癌的Ⅲ期临床研究[J].临床肿瘤学杂志,2010,15(6):545-548.
[7]周国亮,宋翼升,辛艳飞,等.灵芝多糖抗氧化和抗肿瘤活性的研究进展[J].中华中医药学刊,2014,32(5):1002-1005.
[8]刘红雨,陈军.肺癌转移进展[J].中国肺癌杂志,2008,11(1):40-42.
[9]彭丽姿,郑美蓉.非小细胞肺癌中EGFR基因突变及靶向药物治疗研究进展[J].医疗装备,2018,31(11):203-204.
[10]施博文,乔文亮,韩玉栋,等.非小细胞肺癌免疫治疗的研究进展[J].现代生物医学进展,2016,16(20):3969-3973.
[11]李婧文,周长林.多糖的免疫调节作用及多糖药物的研究进展[J].中国生化药物杂志,2016,4(36):24-28.
[12]涂雪松,黄福恩,瞿广桥,等.人参复方多糖对老年晚期非小细胞肺癌患者免疫功能和生活质量的影响[J].医学综述,2016,22(8):1659-1664.
[13]杨美菊,程哲.香菇多糖联合多西他赛与奈达铂化疗治疗肺结核合并非小细胞肺癌的临床疗效研究[J].癌症进展,2017,15(5):518-520.
[14]王洁茹,王金英,张婷婷,等.黄芪多糖调节黑色素瘤小鼠PD-1/PD-Ls分子表达的研究[J].上海中医药大学学报,2014,25(5):74-79.
[15]钟理,蒋德昭,王绮如.灵芝复方剂对K562白血病细胞增殖、分化的影响[J].湖南医科大学学报,1999,24(6):521-524.
[16]林志彬.灵芝抗肿瘤作用的免疫学机制及其临床应用[J].中国药理学与毒理学杂志,2015,29(6):865-882.
[17]熊川,罗强,金鑫,等.人工栽培灵芝中多糖的部分理化性质及免疫调节作用[J].微生物学通报,2018,45(4):825-835.
[18]陈源红,邹佳峻,李松波.灵芝多糖对人肝癌细胞Hep G2增殖及体外迁移的影响[J].广东医学,2018,39(11):1625-1628.
[19]梁曾恩妮.灵芝多糖对结肠癌细胞增殖抑制和凋亡的影响初步研究[D].长沙:湖南农业大学,2014.