详细信息
黄芩苷对胃癌BGC-823、MGC-803细胞迁移能力的影响 被引量:4
Effects of Baicalin on the Migration Ability of Gastric Carcinoma Cells BGC-823 and MGC-803
文献类型:期刊文献
中文题名:黄芩苷对胃癌BGC-823、MGC-803细胞迁移能力的影响
英文题名:Effects of Baicalin on the Migration Ability of Gastric Carcinoma Cells BGC-823 and MGC-803
作者:王宏伟[1];徐燕[2];李海龙[2,3];陈凤琴[4];吴红彦[2,3]
第一作者:王宏伟
机构:[1]甘肃中医药大学附属医院,甘肃兰州730000;[2]甘肃中医药大学,甘肃兰州730000;[3]甘肃省中医方药挖掘与创新转化重点实验室甘肃省中药新产品创制工程实验室,甘肃兰州730000;[4]兰州大学第二医院,甘肃兰州730000
第一机构:甘肃中医药大学第二附属医院
年份:2016
卷号:23
期号:8
起止页码:64
中文期刊名:中国中医药信息杂志
外文期刊名:Chinese Journal of Information on Traditional Chinese Medicine
收录:CSTPCD;;CSCD:【CSCD_E2015_2016】;
基金:甘肃省自然科学基金(148RJZA073)
语种:中文
中文关键词:脂多糖;Toll;样受体;黄芩苷;迁移;胃癌
外文关键词:LPS; Toll-like receptor; baicalin; migration; gastric carcinoma
摘要:目的观察黄芩苷对胃癌BGC-823、MGC-803细胞迁移的影响,探讨其可能的作用机制。方法划痕实验和Transwell小室观察Toll样受体(TLR)激活后以及黄芩苷干预TLR激活后胃癌BGC-823、MGC-803细胞迁移能力;RT-q PCR和Western blot检测胃癌BGC-823、MGC-803细胞的TLR4、激活蛋白-1(AP-1)、血管内皮生长因子(VEGF)m RNA和蛋白表达。结果脂多糖(LPS)可促进胃癌BGC-823、MGC-803细胞迁移,黄芩苷可抑制LPS干预后胃癌BGC-823、MGC-803细胞迁移;LPS可上调TLR4、AP-1、VEGF m RNA和蛋白表达,黄芩苷可下调LPS干预后胃癌BGC-823、MGC-803细胞的TLR4、AP-1、VEGF m RNA和蛋白表达。结论黄芩苷可阻断TLR4-AP-1-VEGF的激活,从而抑制胃癌BGC-823、MGC-803细胞的迁移。
Objective To explore the effects of baicalin on the migration of gastric carcinoma cells BGC-823 andMGC-803; To discuss the possible mechanism of baicalin on migration. Methods Scratch test and Transwell chamberwere utilized to observe the effects of activation of Toll-like receptor (TLR) and the migration of BGC-823 andMGC-803 after baicalin intervention. RT-qPCR and Western blot were used to detect mRNA and protein expressionsof TLR4, AP-1 and VEGF of BGC-823 and MGC-803. Results LPS could promote migration in both BGC-823 andMGC-803, but baicalin could inhibit the migration of BGC-823 and MGC-803 after the intervention of LPS; LPScould up-regulate mRNA and protein expressions of TLR4, AP-1 and VEGF, while baicalin could inhibit proteinexpressions of TLR4, AP-1 and VEGF. Conclusion Baicalin can inhibit migration of gastric carcinoma cellsBGC-823 and MGC-803 by blocking the activation of TLR4-AP-1-VEGF pathway.
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