青龙衣多糖对结肠癌HCT-116细胞增殖、凋亡及PI3K/Akt信号通路的影响  

Effects of Juglandis Immaturum Exocarpium Polysaccharide on Proliferation,Apoptosis and PI3K/Akt Signaling Pathway of Human Colon Carcinoma Cell Line HCT-116

作　　者：胡泽成[1] 

机构地区：[1]南华大学附属第一医院,湖南衡阳421000

出　　处：《中国实验方剂学杂志》2016年第18期136-139,共4页Chinese Journal of Experimental Traditional Medical Formulae

基　　金：吉林省教育厅"十二五"科学技术研究项目(吉教科合字2014第203号)

摘　　要：目的:从磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)信号通路方面探讨青龙衣多糖对结肠癌HCT-116细胞增殖、凋亡的影响。方法:青龙衣多糖(10,20,50,100 mg·L-1)处理处于对数生长期的HCT-116细胞,另设空白组,MTS法检测24,48,72,96 h后的细胞增殖抑制率,PI单染法,Annexin-FITC/PI双染法分别检测48 h后细胞周期及细胞凋亡情况,蛋白质免疫印迹(Western blot)法检测48 h后Akt及p-Akt蛋白表达水平。结果:青龙衣多糖对HCT-116细胞的增殖具有明显的抑制作用,呈剂量依赖和时间依赖效应;与空白组比较,各处理组G0/G1期细胞比例增加,S期和G2/M期细胞比例下降,且各质量浓度间的差异具有统计学意义(P<0.05);与空白组比较,除10 mg·L-1组外,其余组早期凋亡率均有显著性增加,而各剂量组的晚期凋亡率及总凋亡率均明显升高,且各质量浓度间的凋亡率均具有统计学意义(P<0.05);与空白组比较,各给药组p-Akt/Akt明显降低,且各质量浓度间p-Akt/Akt差异具有统计学意义(P<0.05)。结论:青龙衣多糖在体外可直接抑制或杀伤人结肠癌HCT-116细胞,具有较强的增殖抑制及诱导凋亡能力,其抗肿瘤机制可能与PI3K/Akt信号通路相关。Objective： To explore the effects of Juglandis Immaturum Exocarpium polysaccharide（ JIP）on the proliferation,apoptosis and phosphatidylinositol 3＇-OH kinase / protein kinase B（ PI3 K / Akt） signaling pathway of human colon carcinoma cell line HCT-116. Method： The HCT-116 cells in logarithmic growth phase were treated with JIP（ 10,20,50,100 mg·L- 1）,and another blank group was set up. The inhibition rates of proliferation at 24,48,72,96 h post-treatment were measured by MTS assay. The cell cycle and apoptosis rate at48 h post-treatment were detected by PI single staining and Annexin-FITC / PI double staining methods,and the protein levels of Akt and p-Akt at 48 h post-treatment were detected by Western blot assay. Result： JIP presented significant inhibitory effect on HCT-116 cell proliferation in a dose-and time-dependent manner. As compared with the blank group,the cells ratio in G0/ G1 phase was increased and cells ratio in S phase and G2/ M phase was declined with significant differences in various groups（ P 0. 05）. As compared with the blank group,the early apoptosis rate of JIP in all the groups except 10 mg·L- 1group was significantly increased,and the apoptosis rate of late phase and total apoptosis rate in various groups were significantly increased with statistical significance（ P 0. 05）. As compared with the blank group,the ratio of p-Akt / Akt was decreased in various treatment groups,andthere was statistically significant difference in ratio of p-Akt / Akt between various concentrations（ P 0. 05）.Conclusion： JIP can directly inhibit or kill human colon cells HCT-116 cells in vitro,and present ability to inhibit proliferation and induce apoptosis. The mechanism might associated with PI3 K / Akt signaling pathway.

关 键 词：青龙衣多糖 结肠癌 增殖 凋亡 磷脂酰肌醇3激酶/蛋白激酶B 

分 类 号：R285.5[医药卫生—中药学]