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作 者:万泽浩 王丁悦 芦梓楠 冯修来 米日亚·买明 依力夏提·马木提 吕红博[6] WAN Ze-hao;WANG Ding-yue;LU Zi-nan;FENG Xiu-lai;Miriya·Maiming;Yilixiati·Mamuti;LYU Hong-bo(Department of Pediatric Cardiothoracic Surgery,the First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054,Xinjang,China;不详)
机构地区:[1]新疆医科大学第一附属医院小儿心胸外科,新疆乌鲁木齐830054 [2]中国医科大学第一附属医院超声科,辽宁沈阳110001 [3]新疆医科大学附属肿瘤医院肿瘤防治研究所,新疆乌鲁木齐830011 [4]新疆医科大学第一附属医院超声科,新疆乌鲁木齐830011 [5]新疆医科大学附属肿瘤医院影像中心,新疆乌鲁木齐830011 [6]新疆医科大学附属肿瘤医院胸外科,新疆乌鲁木齐830011
出 处:《广东医学》2022年第7期855-859,共5页Guangdong Medical Journal
基 金:国家级大学生创新计划基金(201910760023)。
摘 要:目的观察番茄碱对人食管癌Eca-109细胞增殖和凋亡的影响,并探讨其中相关分子机制。方法采用CCK-8法检测不同浓度(1、2、3、4、5、6、7、8、9μmol/L)番茄碱对食管癌Eca-109细胞增殖抑制率的影响;采用流式细胞术和Western Blot蛋白质印迹法分别测定不同浓度(0、1.5、3、6μmol/L)番茄碱诱导食管癌Eca-109细胞的凋亡率及其核因子-κB(NF-κB)p65、血管内皮生长因子(VEGF)蛋白相对表达量。结果通过CCK-8法观察到,番茄碱呈剂量依赖性地抑制食管癌Eca-109细胞的增殖活性,差异有统计学意义(P<0.001),其时间依赖性低,差异无统计学意义(P>0.05),当番茄碱浓度>6μmol/L时,食管癌Eca-109细胞几乎不能存活。在含番茄碱浓度3、6μmol/L培养基中培养食管癌Eca-109细胞24 h后,细胞早期、晚期和总体凋亡率增加,差异有统计学意义(P<0.05),且伴随NF-κB p65、VEGF蛋白表达水平降低,差异有统计学意义(P<0.001)。结论番茄碱在体外细胞实验中,可以抑制食管癌Eca-109细胞的增殖,并促进其早期、晚期凋亡,其作用机制可能与下调肿瘤增殖生长相关蛋白NF-κB与VEGF相关。Objective To observe the influences of tomatidine(TOM)on the proliferation and apoptosis of human esophageal cancer Eca-109 cells,and to investigate the related molecular mechanisms.Methods CCK-8 method was used to assess the influence of different concentrations of TOM on the proliferation inhibition rate of esophageal carcinoma Eca-109 cells.The apoptosis rate and relative expression of nuclear factor-κB(NF-κB)p65 and vascular endothelial growth factor(VEGF)in Eca-109 cells induced by TOM were determined by flow cytometry and Western Blot.Results According to CCK-8 results,TOM significantly inhibited the proliferation of esophageal cancer Eca-109 cells(P<0.001),but it didn′t have much correlation with time(P>0.05).When the concentration of TOM was greater than 6μmol/L,Eca-109 cells in esophageal cancer were rarely viable.After treated with 3 and 6μmol/L TOM for 24 h,the early,late and total apoptosis rates of Eca-109 cells were significantly increased(P<0.05),and the protein expression levels of NF-κB p65 and VEGF were significantly reduced(P<0.001).Conclusion TOM can inhibit the proliferation and promote the early and late apoptosis of esophageal cancer Eca-109 cells in vitro.Down-regulation of NF-κB and VEGF may be the cause.
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