去甲斑蝥酸钠通过抑制PI3K/Akt通路诱导胰腺癌细胞凋亡的机制研究  

Mechanism of sodium norcantharidate inducing apoptosis of pancreatic cancer cells through PI3K/Akt pathway

作　　者：陈慕媛 张关亭[1] 吕孝朋 赵丽 CHEN Mu-yuan;ZHANG Guan-ting;LV Xiao-peng;ZHAO Li(Laboratory of Henan Institute of Traditional Chinese Medicine,Zhengzhou Henan 450006,China;Clinical Laboratory of Zhengzhou Institute of Occupational Disease Control,Zhengzhou Henan 450053,China;Aidikang Medical Laboratory,Zhengzhou Henan 450000,China)

机构地区：[1]河南省中医药研究院检验科,河南郑州450006 [2]郑州市职业病防治院临检科,河南郑州450053 [3]艾迪康医学检验中心,河南郑州450000

出　　处：《毒理学杂志》2020年第2期143-146,149,共5页Journal of Toxicology

基　　金：河南省科技厅科技攻关项目(132102310493)。

摘　　要：目的探究去甲斑蝥酸钠(SNCTD)通过PI3K/Akt信号通路诱导胰腺癌PANC-1细胞凋亡的机制。方法体外培养人胰腺癌细胞(PANC-1),实验分别给予浓度为0、10、30和90μmol/L的SNCTD处理,采用MTT法检测PANC-1细胞活力,并计算生长抑制率,流式细胞术检测凋亡情况;Western blot检测p-PI3K、p-Akt、Bcl-2、Bax和Caspase-3蛋白表达水平。结果与对照组相比,10、30和90μmol/L SNCTD组PANC-1细胞活力依次降低,S期和G2/M期细胞比例依次降低,凋亡率依次升高,p-PI3K、p-Akt和Bcl-2蛋白表达水平明显降低,而Bax和Caspase-3蛋白表达水平升高,差异均有统计学意义(P<0.05)。结论 SNCTD可促进胰腺癌细胞凋亡,其作用机制可能是抑制PI3K/Akt通路,进而下调Bcl-2蛋白,上调Bax和Caspase-3蛋白表达有关。Objective To investigate the proper mechanism of apoptosis of PANC-1 cells induced by sodium norcantharidate(SNCTD) through PI3 K/Akt signaling pathway. Methods Human pancreatic cancer cells(PANC-1) were cultured in vitro, and treated with SNCTD at concentrations of 0, 10, 30 and 90 μm respectively, cell viability of PANC-1 cells was detected by MTT method, the growth inhibition rate was calculated, apoptosis was detected by flow cytometry;and Western blot was used to detect the expression levels of p-PI3 K, p-Akt, Bcl-2, Bax and Caspase-3 proteins. Results Compared with control group, the growth activity of SNCTD-treated PANC-1 cells were decreased gradually in a dose-dependent manner. The ratio of G0/G1 phase cells were increased gradually, while the number of S-phase cells and G2/M cells were decreased. Moreover, apoptosis rate of SNCTD-treated PANC-1 cells was increased significantly(P<0.05);compared with the control group, the expressions of p-PI3 K, p-Akt and Bcl-2 proteins in SNCTD-treated PANC-1 cells decreased significantly, while Bax and Caspase-3 protein levels increased significantly(P<0.05). Conclusion SNCTD can promote the apoptosis of pancreatic cancer cells, which may be related to the inhibition of PI3 K/Akt pathway activity, then down-regulating Bcl-2 and up-regulating Bax and Caspase-3 protein expressions.

关 键 词：胰腺癌细胞 去甲斑蝥酸钠 PI3K/AKT通路 细胞凋亡 

分 类 号：R735.9[医药卫生—肿瘤] R99[医药卫生—临床医学]