摘要
目的探索宝藿苷Ⅰ(baohuoside I,BI)对子宫内膜癌Ishikawa细胞的诱导凋亡作用及其相关的分子机制。方法以0μM及0 h未处理均作为空白对照组,BI处理(3、10、20、30、40μM及3、6、12和24 h)后作为实验组;宝藿苷Ⅰ对Ishikawa细胞的增殖抑制作用通过CCK-8实验检测;宝藿苷Ⅰ对Ishikawa细胞的诱导凋亡作用和线粒体膜电位变通过Flow cytometry检测;通过蛋白免疫印迹实验检测细胞凋亡和信号通路相关蛋白。结果CCK-8实验表明宝藿苷Ⅰ能以浓度梯度(3、10、20、30、40μM)有效抑制Ishikawa细胞的增殖(存活率分别为89.56±0.96、74.69±1.21、60.28±1.09、43.51±2.17),且对正常细胞的毒副作用低于5-FU。流式细胞术结果显示宝藿苷Ⅰ能通过降低线粒体膜电位水平,有效诱导Ishikawa细胞凋亡,各组凋亡细胞比例为(9.92±0.77)%、(14.01±0.83)%、(17.05±1.41)%、(28.21±1.73)%和(44.55±3.11)%。Western blot实验结果表示,宝藿苷Ⅰ能上调p-p38的水平并降低p-STAT3的水平。结论宝藿苷Ⅰ能高效降低Ishikawa的细胞活性,并通过降低线粒体膜电位,激活线粒体依赖性途径诱导其凋亡,其调节机制是通过激活p38信号通路并抑制STAT3通路来实现的。
Objective To investigate the apoptosis-inducing effect of baohuoside I(BI)on endometrial cancer Ishikawa cells and its related molecular mechanism.Methods With 0μM and 0 h treatment were used as blank control group,and BI treatment was used as experimental group.The inhibitory effect of BI on the proliferation of Ishikawa cells was detected by CCK-8 assay.The apoptosis-inducing effect of BI on Ishikawa cells and the changes of mitochondrial membrane potential were detected by flow cytometry.The expressions of apoptosis-related proteins and signaling pathway-related proteins were detected by Western blot.Results CCK-8 experiment showed that BI could be expressed in concentration gradient(3,10,20,30,40μM).It could effectively inhibit the proliferation of Ishikawa cells(the survival rates were 89.56±0.96,74.69±1.21,60.28±1.09 and 43.51±2.17 respectively).Its toxic and side effects on normal cells were lower than that of 5-FU.The results of flow cytometry showed that BI could effectively induce the apoptosis of Ishikawa cells by reducing the level of mitochondrial membrane potential.The proportion of apoptotic cells in each group was(9.92±0.77)%,(14.01±0.83)%,(17.05±1.41)%,(28.21±1.73)%and(44.55±3.11)%.Western blot showed that BI could up-regulate the level of p-p38 and reduce the level of p-STAT3.Conclusions BI can effectively inhibit the proliferation of Ishikawa cells,and induce apoptosis by reducing the mitochondrial membrane potential and activating the mitochondria-dependent pathway.Its regulatory mechanism is achieved by activating the p38 signaling pathway and inhibiting the STAT3 pathway.
作者
康丽荣
张林爱
张婧
吕卫琴
赵瑞霞
Kang Lirong;Zhang Linai;Zhang Jing;Lyu Weiqin;Zhao Ruixia(Department of Family Planning,Shanxi Maternal and Child Health Hospital,Taiyuan 030013,China;Yuncheng Central Hospital,Yuncheng 044099,China;Department of Gynaecology,Shanxi Provincial Cancer Hospital,Taiyuan 030013,China)
出处
《中华内分泌外科杂志》
CAS
2022年第3期330-334,共5页
Chinese Journal of Endocrine Surgery
基金
山西省卫生健康委科研课题(2018156)。
