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作 者:郭巍[1] 张秋雨[1] 刘明清[1] 徐智广[1] GUO Wei;ZHANG Qiu-yu;LIU Ming-qing;XU Zhi-guang(Department of Health Management and Services, Cangzhou Medical College, Cangzhou 061001, China)
出 处:《现代食品科技》2019年第8期21-26,共6页Modern Food Science and Technology
基 金:河北省科技计划项目(16277752D)
摘 要:本文探究了银杏叶提取物对甲状腺癌细胞增殖、凋亡作用的影响。将培养后的细胞分为空白组、低浓度银杏叶组、中浓度银杏叶组、高浓度银杏叶组,观察四组细胞增殖、凋亡、侵袭、迁移和粘附能力,并对凋亡相关蛋白p53、B淋巴细胞瘤-2基因(Bcl-2)、Bax表达进行检测。研究结果显示,72 h时高浓度银杏叶组细胞增殖率为14.25%,低于其他三组;凋亡率为81.64%,高于其他三组。高浓度银杏叶组甲状腺癌细胞迁移数、侵袭数、粘附数分别为25.66、24.19、13.02,均低于其他三组(p<0.05)。高浓度银杏叶组甲状腺癌细胞p53、Bcl-2相对表达量分别为0.36、0.26,均低于其他三组,Bax相对表达量为1.79,高于其他三组(p<0.05)。结果表明银杏叶提取物能够抑制甲状腺癌细胞增殖、侵袭、迁移、粘附能力,还能够通过调控凋亡相关蛋白p53、Bcl-2、Bax表达而促进细胞凋亡,且其能力呈现浓度依赖性。To investigate the effects of Ginkgo biloba extract on proliferation and apoptosis of thyroid cancer cells. The cultured cells were divided into blank group, low concentration ginkgo leaf group, medium concentration ginkgo leaf group and high concentration ginkgo leaf group. The proliferation, apoptosis, invasion, migration and adhesion ability of the four groups were analyzed, and the expression of apoptosis-related protein p53, B lymphoma-2 gene(Bcl-2) and Bax were detected. The results showed that the cell proliferation rate and apoptotic rate of high concentration Ginkgo biloba leaves group at 72 h were 14.25%, lower than that of the other three groups, and 81.64%, higher than those of the other three groups, respectively. The number of migration, invasion and adhesion of thyroid cancer cells in the high concentration Ginkgo biloba group were 25.66, 24.19, 13.02, respectively, lower than that of the other three groups(p<0.05). The relative expression of p53 and Bcl-2 in thyroid cancer cells of high concentration Ginkgo biloba leaves group were 0.36 and 0.26, respectively, lower than that of the other three groups. The relative expression of Bax in high concentration Ginkgo biloba leaves group was 1.79, higher than that of the other three groups(p<0.05). Ginkgo biloba extract can inhibit the proliferation, invasion, migration and adhesion of thyroid cancer cells, and promote cell apoptosis by regulating the expression of apoptosis-related proteins p53, Bcl-2 and Bax in a concentration-dependent manner.
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