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猕猴桃根多糖对人胃癌SGC-7901细胞增殖、凋亡及p-p38表达的影响
引用本文:宋文瑛,许冠华,张光霁.猕猴桃根多糖对人胃癌SGC-7901细胞增殖、凋亡及p-p38表达的影响[J].中国中西医结合杂志,2014,34(3):0329-333.
作者姓名:宋文瑛  许冠华  张光霁
作者单位:浙江中医药大学基础研究院(杭州 310053)
基金项目:国家自然科学基金资助项目(No.81273904);浙江省自然科学基金资助项目(No.Y2100827)
摘    要:目的探讨猕猴桃根多糖(Actinidia chinensis Planch polysaccharid,ACPS)对人胃腺癌细胞(SGC-7901)增殖和凋亡的影响,及对SGC-7901细胞磷酸化p38(p-p38)蛋白表达的影响。方法采用CCK-8检测不同浓度ACPS对SGC-7901细胞的24、48、72h的抑制作用;流式细胞技术检测各浓度ACPS作用48h后SGC-7901细胞凋亡的发生率;Western blot法检测各浓度ACPS作用SGC-7901细胞后前体半胱氨酰天冬氨酸酶-9(pro-caspase-9)、聚腺苷二磷酸核糖聚合酶(PARP)和p-p38蛋白量的表达,以及p38特畀性抑制剂预处理细胞后pro-caspase-9、PARP和p-p38蛋白量的表达。结果与对照组比较,1、2.5、5、10mg/mLACPS作用胃癌SGC.7901细胞后吸光度下降(P〈0.05);同时药物剂量越高,作用时间越长,吸光度越低(P〈0.01);24、48、72hIC50分别为7.43、3.88、1.32mg/mL;ACPS能下调SGC-7901细胞中pro-caspase-9蛋白的表达(P〈0.01),增加PARP剪切蛋白的表达(P〈0.01);进一步研究发现,ACPS处理SGC-7901细胞24h后,p38的磷酸化水平升高(P〈0.05),p38特异性抑制剂处理细胞2h后能抑制p38磷酸化表达,并能抑制ACPS诱导的细胞凋亡。结论ACPS具有抑制人胃癌SGC-7901细胞增殖,诱导其凋亡的作用;激活p38途径,进而激活caspase-9和PARP,最终导致细胞死亡,可能是其诱导胃癌细胞凋亡的分子机制之一。

关 键 词:猕猴桃根多糖  SGC-7091细胞  细胞凋亡  p38丝裂原活化蛋白激酶

Effect ofActinidia chinensis Planch Polysaccharide on the Growth and Apoptosis,and p-p38 Ex-pression in Human Gastric Cancer SGC-7901 Cells
Authors:SONG Wen-ying  XU Guan-hua  andZHANG Guang-ji
Institution:1 Institute of Basic Theory of Traditional Chinese Medicine, Zhejiang University of Chinese Medicine, Hangzhou 310053, China;2 First College of Clinical Medicine, Zhejiang University of Chinese Medicine, Hangzhou 310053, China)
Abstract:Objective To investigate the effect of Actinidia chinensis Planch polysaccharide (ACPS) on the growth and apoptosis of human gastric cancer SGC-7901 cells, and to explore the effect of SGC-7901 cells on p-p38 expression. Methods The inhibition rates at different concentrations of ACPS on SGC-7901 cells at 24, 48, and 72 h were detected using CCK-8 method. Apoptosis ratios in SGC-7901 were determined by flow cytometry after 48-h treatment of different concentrations of ACPS. The expression of pro-caspase-9, PARP, and p-p38 in SGC-7901 cells after treated by different concen- trations of ACPS was detected using Western blot. The expression of pro-caspase-9, PARP, and p-p38 was detected after SGC-7901 cells were pre-treated by p38 specific inhibitor. Results Compared with the control group, the optical density of SGC-7901 cells decreased after treated by 1, 2.5, 5, and 10 mg/mL ACPS (P 〈0.05). Meanwhile, the longer the acting time, the lower the optic density (P 〈0.01 ). IC5o was 7.43 mg/mL at 24 h; 3.88 mg/mL at 48 h, and 1.32 mg/mL at 72 h respectively. ACPS sup- pressed the protein expression of pro-caspase-9 (P 〈0.01 ) and up-regulated the expression of PARP (89KD) (both P 〈0.01 ). Further study showed that the protein expression of p-p38 was up-regulated in SGC-7901 cells treated by ACPS of different concentrations at 24 h (P 〈0.05). The expression of phos- phorylation p38 and the ACPS induced apoptosis of SGC-7901 cells could be inhibited after treated by specific inhibitor for 2 h. Conclusions ACPS could inhibit the growth of SGC-7901 cells and induce apop- tosis. The underlying mechanism of inducing apoptosis was partially due to activating the p38MAPK path and further activating Caspase9 and PARP, finally leading to cell death.
Keywords:Actinidia chinensis Planch polysaccharide  SGC-7901 cell  apoptosis  p38 mitogenactivated protein kinase
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