山东大学学报 (医学版) ›› 2019, Vol. 57 ›› Issue (6): 68-74.doi: 10.6040/j.issn.1671-7554.0.2018.1443
• • 上一篇
罗梦颖1,吴蓓2,王叶1,骆衡3,4,曹煜1
LUO Mengying1, WU Bei2, WANG Ye1, LUO Heng3,4, CAO Yu1
摘要: 目的 研究芳姜黄酮对子宫颈癌SiHa细胞体外增殖、迁移与侵袭的作用,并初步探讨其机制。 方法 体外培养SiHa细胞,不同浓度芳姜黄酮(0、20、40、80 mg/L)作用于细胞后,采用CCK8法检测SiHa细胞体外增殖情况;吉姆萨染色显微镜观察SiHa细胞凋亡情况;细胞划痕实验和Transwell小室检测SiHa细胞体外迁移和侵袭能力;流式细胞术分析确定SiHa细胞的诱导凋亡率;Western blotting检测SiHa细胞MMP2、MMP9及p53蛋白表达。 结果 芳姜黄酮可抑制SiHa细胞的体外增殖(F浓度=162.419,P<0.001;F时间=99.442,P<0.001;F浓度×时间=2.111,P=0.095)、迁移(F浓度=432.158,P<0.001;F时间=528.845,P<0.001)和侵袭(F浓度=434.362,P<0.001),且与其浓度、作用时间呈正相关;流式细胞仪分析表明,芳姜黄酮可诱导SiHa细胞凋亡(F浓度=482.690,P<0.001),且与其浓度呈正相关;Western blotting检测结果表明,经芳姜黄酮处理后,凋亡相关蛋白p53的表达明显上调(F浓度=2.086,P=0.045)、侵袭和转移相关蛋白MMP2、MMP9的表达下调(F浓度=18.906,P=0.001;F浓度=9.847,P=0.005)。 结论 芳姜黄酮具有抑制SiHa细胞体外增殖及诱导细胞凋亡的能力,其机制可能与调节凋亡相关蛋白p53表达有关;芳姜黄酮可能通过调节侵袭和转移相关蛋白MMP2、MMP9的表达,进而抑制SiHa细胞迁移与侵袭。
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