天津医药

天津医药 ›› 2019, Vol. 47 ›› Issue (10): 1020-1025.doi: 10.11958/20190272

• 细胞与分子生物学 • 上一篇    下一篇

高良姜素通过PI3K/Akt及p38-MAPK信号通路增强胃癌SGC-7901细胞对阿帕替尼的敏感性

贺文煜，张海明，袁昌劲△   

  1. 华中科技大学同济医学院附属武汉中心医院中西医结合肿瘤科（邮编430014）
  • 收稿日期:2019-01-28 修回日期:2019-08-01 出版日期:2019-10-15 发布日期:2019-11-11
  • 通讯作者: 袁昌劲 E-mail:3367205751@qq.com
  • 基金资助:
    武汉市中心医院院内科研基金研究项目

Galangin enhanced antitumor effects of apatinib in gastric cancer SGC-7901 cells via PI3K/Akt and p38-MAPK signaling pathway

HE Wen-yu, ZHANG Hai-ming, YUAN Chang-jin△   

  1. Department of Combines Traditional Chinese and Western Internal Medicine, the Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China
  • Received:2019-01-28 Revised:2019-08-01 Published:2019-10-15 Online:2019-11-11
  • Supported by:
     

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摘要： 摘要：目的 探讨高良姜素对阿帕替尼抗胃癌作用的影响及可能机制。方法 体外培养胃癌SGC-7901细胞， 3-（4,5-二甲基噻唑-2）-2,5-二苯基四氮唑溴盐（MTT）法筛选出高良姜素和阿帕替尼抑制胃癌细胞增殖的合适浓 度。将胃癌细胞分为4组：空白对照组、高良姜素组、阿帕替尼组和高良姜素+阿帕替尼组。MTT法检测细胞增殖活 力；流式细胞术检测细胞凋亡率；细胞划痕实验和Transwell小室实验分别检测细胞迁移和侵袭能力；Western blot检 测细胞凋亡及PI3K/Akt及p38-MAPK信号通路相关蛋白表达。结果 阿帕替尼和高良姜素均显著抑制胃癌SGC- 7901细胞的增殖，并呈浓度依赖性（P＜0.05），20 mg/L阿帕替尼和300 mg/L高良姜素是最佳的干预浓度。与20 mg/L 阿帕替尼组相比，高良姜素+阿帕替尼组可以明显抑制胃癌SGC-7901细胞的增殖、迁移和侵袭（P＜0.05）。流式细 胞术结果显示，高良姜素+阿帕替尼组对胃癌SGC-7901细胞促凋亡作用明显优于20 mg/L阿帕替尼组（P＜0.05）。 Western blot结果显示，高良姜素+阿帕替尼组Bcl-2相关X蛋白（Bax）、磷酸化蛋白激酶B（p-Akt）、磷酸化丝裂原活 化蛋白激酶（p-p38）蛋白表达明显高于20 mg/L阿帕替尼组，B淋巴细胞瘤-2（Bcl-2）蛋白明显低于20 mg/L阿帕替尼 组（P＜0.05）。结论 高良姜素可能通过抑制PI3K/Akt和激活p38-MAPK信号通路增强阿帕替尼抗胃癌SGC-7901 细胞的作用。

关键词: 高良姜素, 胃肿瘤, 阿帕替尼, 抗肿瘤作用, PI3K/Akt信号通路, p38-MAPK信号通路

Abstract: Abstract: Objective To explore the influence of galangin in the antitumor effect of apatinib in gastric cancer cells and the underlying mechanism. Methods Human gastric cancer cell line SGC-7901 was cultured in vitro, and the satisfactory concentration of galangin and apatinib against SGC-7901 cells were determined by MTT assay. Gastric cancer cells were assigned to four groups: blank control group, galangin group, apatinib group and galangin+ apatinib group. Cell proliferation was determined by MTT assay, cell apoptosis was determined by flow cytometry assay, the migration and invasion of SGC-7901 cells were detected by wound healing and Transwell assay, respectively. Meanwhile, the expressions of related proteins were measured by Western blot assay. Results Both galangin and apatinib could significantly inhibit the proliferation of SGC-7901 cells in a dose-dependent manner (P＜0.05). Compared with apatinib group there was an enhanced inhibitory effects on cell proliferation, migration and invasion in galangin+apatinib group (P＜0.05). There was a significant promoted apoptosis in the galangin + apatinib group compared with that of 20 mg/L apatinib group (P＜0.05). Western blot showed that the expression levels of Bax, p-Akt and p-p38 were increased, and the level of Bcl-2 protein was significantly decreased, in galangin + apatinib group comparison with those of 20 mg / L apatinib group (P＜0.05). Conclusion Galangin can enhance antitumor effects of apatinib on gastric cancer SGC-7901 cells by inhibiting PI3K/Akt and activating p38-MAPK signaling pathway.

Key words: Galangin, stomach neoplasms, Apatinib, anti-cancer, PI3K/Akt signaling pathway, p38-MAPK signaling pathway

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