棕矢车菊素对胃癌细胞增殖、凋亡和血管生成拟态的影响及作用机制实验研究  

Effects of jaceosidin on proliferation,apoptosis and vasculogenic mimicry of gastric cancer cells and its mechanisms

作　　者：孙波 周雷[1] 王小龙[1] 吕莹[1] 张海兵[1] 屠佳佳 冯辉 SUN Bo;ZHOU Lei;WANG Xiaolong;LYU Ying;ZHANG Haibing;TU Jiajia;FENG Hui(Shuyang Hospital Affiliated to Nanjing University of Chinese Medicine,Shuyang 223600,China)

机构地区：[1]南京中医药大学附属沭阳医院,江苏沭阳223600

出　　处：《陕西医学杂志》2024年第11期1463-1467,共5页Shaanxi Medical Journal

基　　金：国家自然科学基金资助项目(81860218)。

摘　　要：目的:探讨棕矢车菊素对胃癌细胞增殖、凋亡和血管生成拟态(VM)的影响及作用机制。方法:采用不同浓度棕矢车菊素(0、10、20、40、80、160μmol/L)作用于人胃癌细胞HGC-27,检测细胞存活率,根据半抑制浓度(IC 50)值选择10、20、40μmol/L棕矢车菊素进行后续实验。将HGC-27细胞随机分为Control组(无干预)、棕矢车菊素-L(加入10μmol/L棕矢车菊素培养)组、棕矢车菊素-M(加入20μmol/L棕矢车菊素培养)组、棕矢车菊素-H(加入40μmol/L棕矢车菊素培养)组和棕矢车菊素-H+K6PC-5(加入40μmol/L棕矢车菊素+10μmol/L SphK1激动剂K6PC-5培养)组。采用平板克隆形成实验检测细胞克隆形成能力,流式细胞术检测细胞凋亡情况,血管形成实验检测各组细胞管状结构形成情况,Western blot检测细胞SphK1和S1P蛋白表达。结果:相较于Control组,棕矢车菊素-L组、棕矢车菊素-M组、棕矢车菊素-H组细胞克隆形成数量、管状结构形成数目及细胞中SphK1和S1P蛋白表达水平逐渐降低,而细胞中管状结构损坏程度增加,细胞凋亡率逐渐升高(均P<0.05)。在高浓度棕矢车菊素的基础上加入K6PC-5逆转了以上指标的变化趋势(均P<0.05)。结论:棕矢车菊素能够抑制胃癌细胞增殖和VM发生,并促进其凋亡,其作用机制可能与下调SphK1/S1P信号通路有关。Objective:To explore the effects of jaceosidin on the proliferation,apoptosis and vasculogenic mimicry(VM)of gastric cancer cells and its underlying mechanisms.Methods:Human gastric cancer cells HGC-27 were treated with various concentrations of jaceosidin(0,10,20,40,80,160μmol/L)and cell survival rate was detected,and jaceosidin at 10,20 and 40μmol/L was selected for subsequent experiments based on the IC 50 values.HGC-27 cells were randomly divided into the control group(no intervention),jaceosidin-L group(cultured with 10μmol/L jaceosidin),jaceosidin-M group(cultured with 20μmol/L jaceosidin),jaceosidin-H group(cultured with 40μmol/L jaceosidin),and jaceosidin-H+K6PC-5 group(cultured with 40μmol/L jaceosidin+10μmol/L SphK1 activator K6PC-5).The colony formation ability was assessed by the plate colony formation assay.Apoptosis was measured by flow cytometry.The formation of tubular structures was assessed by angiogenesis assay.Western blot was used to detect the expression of SphK1 and S1P proteins in cells.Results:Compared with the control group,the number of cell colonies,the number of tubular structures,and the expression levels of SphK1 and S1P proteins gradually decreased in the jaceosidin-L,jaceosidin-M and jaceosidin-H groups,while the degree of tubular structure damage increased and the rate of apoptosis gradually increased(all P<0.05).The addition of K6PC-5 to the high concentration of jaceosidin reversed the trend of these indicators(all P<0.05).Conclusion:Jaceosidin can inhibit the proliferation and VM of gastric cancer cells and promote their apoptosis,and its mechanism of action may be related to the downregulation of the SphK1/S1P signaling pathway.

关 键 词：胃癌 棕矢车菊素 细胞增殖 细胞凋亡 血管生成拟态 鞘氨醇激酶1/鞘氨醇-1-磷酸信号通路 

分 类 号：R36[医药卫生—病理学]