温郁金二萜类化合物C抗胃癌作用的实验研究  

Curcuma wenyujin Diterpenoid Compound C Fought against Gastric Cancer: an Experimental Study

作　　者：金海峰[1] 吕宾[1] 戴金锋 盛桂琴[1] 

机构地区：[1]浙江中医药大学附属第一医院消化内科,杭州310006

出　　处：《中国中西医结合杂志》2015年第2期216-221,共6页Chinese Journal of Integrated Traditional and Western Medicine

基　　金：国家自然科学青年基金项目(No.81202822);浙江省自然科学基金资助项目(No.Y2110959);浙江省中医药管理局重大攻关项目(No.2007ZGG002)

摘　　要：目的通过肿瘤坏死因子-α(TNF-α)刺激胃癌细胞株SGC7901,探讨p38丝裂原激活的蛋白激酶MAPK(p38MAPK)调控核转录因子(NF)-κB通路在温郁金二萜类化合物C抗炎和诱导胃癌细胞凋亡中的作用。方法将不同浓度的温郁金二萜类化合物C在不同的时间,体外作用于人脐静脉细胞(HUVECs)、胃癌SGC-7901细胞,采用MTT法检测其对两种细胞株的增殖抑制率;采用Annexin V-FITC/PI双染法检测各组胃癌细胞凋亡率;细胞免疫荧光检测p65核转位情况,采用Western blot检测各组p38MAPK/P-p38MAPK、p65/P-p65及Caspase-3/P-Caspase-3蛋白表达量。结果温郁金二萜类化合物C对SGC-7901细胞增殖有明显的抑制作用,并能有效地诱导胃癌细胞SGC-7901凋亡;温郁金二萜类化合物C能一定程度地减少胃癌细胞SGC-7901p65核转位发生;Western blot结果提示,p38MAPK、p65蛋白的表达随着温郁金二萜类化合物C浓度的提高而减少,而Caspase-3蛋白的表达则增加(P<0.05)。结论通过p38MAPK调控p65来激活凋亡执行蛋白Caspase-3是温郁金二萜类化合物C发挥抗炎和抗癌可能的作用机制之一。Objective To study the role of nuclear factor （NF）-KB pathway with p38MAPK in Curcuma wenyujin diterpenoid compound C （CDCC） fighting against inflammation and inducing gastric cancer cell apoptosis by stimulating gastric cell SGC7901 with tumor necrosis factor-eL （TNF-a）. Methods Human umbilical vein endothelial cells （HUVECs） and human gastric cancer SGC-7901 cells were in vitro acted by CDCC in different concentrations at different time points. Their growth inhibition ratios were measured by MIF assay. The apoptosis rate of gastric cancer cells was detected by Annexin V-FITC/PI double staining. Nuclear translocation of p65 was detected by cell immunofluorescence. Expression levels of p38MAPK/P-p38MAPK, p65/P-p65, and Caspase 3/P-Caspase 3 were measured by Western blot. Re sults CDCC had significant inhibitory effect on the proliferation of SGC-7901. It also could effectively induce the apoptosis of gastric cancer cell SGC-7901. It also could reduce nuclear translocation of p65 in gastric cancer cell SGC-7901. Results of Western blot indicated that expression levels of p38MAPK and p65 were reduced and the expression level of Caspase-3 was elevated along with increased concentrations of CDCC（P 〈 0.05）. Conclusion Apoptosis executive protein Caspase 3 activated by regulating p65 via p38MAPK might be one of possible mechanisms for CDCC fighting against inflammation and gastric cancer.

关 键 词：胃癌 温郁金 二萜类化合物 丝裂原活化蛋白激酶 核转录因子-ΚB 细胞凋亡 

分 类 号：R285[医药卫生—中药学]