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作 者:黄莹莹[1] 裴浩[1] HUANG Yingying;PEI Hao(Department of Stomatology,The First Affiliated Hospital of Nanyang Medical College,China,473000)
机构地区:[1]南阳医学高等专科学校第一附属医院口腔科,473000
出 处:《实用口腔医学杂志》2022年第3期327-332,共6页Journal of Practical Stomatology
摘 要:目的:探索鱼藤素(DEG)对舌鳞癌(TSCC)的体外及体内抗癌作用及其作用机制。方法:CCK-8实验检测DEG对舌鳞癌细胞系CAL27细胞的增殖的影响,流式细胞术检测细胞凋亡及活性氧(ROS)水平。构建裸鼠移植瘤模型并分组处理,测量瘤体体积、质量及肿瘤抑制率;TUNEL检测细胞凋亡;Western blot实验检测PI3K/AKT信号通路相关蛋白表达。结果:DEG对CAL27细胞具有增殖抑制和诱导凋亡作用;DEG能够通过上调CAL27细胞中的ROS水平,抑制PI3K/AKT信号通路;体内实验证明DEG能够以浓度依赖性的方式抑制裸鼠移植瘤的生长,相同浓度下抑制效果强于顺铂,30 mg/kg的DEG对瘤体的抑制率高达72.6%。结论:DEG对舌鳞癌细胞具有抑制增殖及诱导凋亡作用,其机制与调节肿瘤细胞中ROS以及PI3K/AKP信号通路有关。Objective:To explore the anti-cancer effects and mechanism of deguelin(DEG)on tongue squamous cell carcinoma(TSCC)in vitro and in vivo.Methods:CCK-8 assay was used to detect the proliferation of TSCC CAL27 cells treated by DEG.Flow cytometry was used to detect cell apoptosis and reactive oxygen species(ROS).In vivo tumor model was established by transplantation of CAL27 cells in 30 nude mice and the mice were divided into 5 groups.After corresponding treatment,the tumor volume,mass and tumor inhibition rate were measured.Tumor cell apoptosis was detected by TUNEL assay.The PI3K/AKT signaling pathway related protein expression was examined by Western blot.Results:DEG inhibited the proliferation and induced the apoptosis of CAL27 cells.DEG inhibited PI3K/AKT signaling pathway by up-regulating ROS levels in CAL27 cells.In vivo experiments showed that DEG inhibited the growth of transplanted tumors in nude mice in a concentration-dependent manner.The inhibitory effect is stronger than that of cisplatin at the same concentration.The inhibitory rate of 30 mg/kg DEG on tumor was as high as 72.6%.Conclusion:DEG can inhibit the proliferation and induce apoptosis of tongue squamous cell carcinoma cells by regolating ROS and PI3K/AKP signling pathway.
关 键 词:鱼藤素 舌鳞状细胞癌 裸鼠移植瘤小鼠 PI3K/AKT信号通路
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