期刊文献+

黄芩苷对脑胶质瘤U251体外增殖、迁移及凋亡的影响

Effects of Baicalin on Proliferation, Migration and Apoptosis of Brain Glioma U251 in Vitro
下载PDF
导出
摘要 目的:研究分析不同浓度黄芩苷对体外培养人脑胶质瘤U251细胞的增殖、迁移及凋亡的作用。方法:以不同浓度的黄芩苷处理神经胶质瘤U251细胞,应用CCK-8、划痕实验、流式细胞仪检测细胞凋亡、Western Blot等细胞学方法检测不同浓度的黄芩苷对细胞增殖、迁移及凋亡及相关蛋白表达的影响。结果:与对照组相比,不同浓度的黄芩苷均能抑制神经胶质瘤U251细胞的增殖和迁移,且抑制作用呈剂量依赖效应,高浓度的黄芩苷能显著抑制胶质瘤细胞的增殖(P<0.01);并且促进U251细胞的凋亡,也呈剂量依赖效应,高浓度的黄芩苷能显著促进胶质瘤细胞的凋亡(P<0.01)。结论:黄芩苷对人胶质瘤细胞U251的增殖和迁移具有抑制作用,凋亡具有促进作用,且抑制及促进效果与药物使用剂量正相关。黄芩苷对于肿瘤治疗效果的研究具有重要意义,有望成为高效抑制肿瘤发生的候选药物。 Objective:To investigate the effects of baicalin in different concentrations on the proliferation,migration and apoptosis of human glioma U251 cells cultured in vitro.Methods:The glioma U251 cells were treated with different concentrations of baicalin.CCK-8,scratches,flow cytometry and Western Blot were used to detect the effects of different concentrations of baicalin on cell proliferation,migration,apoptosis and the expression of related proteins.Results:Compared with the control group,different concentrations of baicalin could inhibit the proliferation and migration of glioma U251 cells,and the inhibitory effect was dose-dependent.High concentration of baicalin could significantly inhibit the proliferation of glioma U251 cells(P<0.01).And the apoptosis of U251 cells was also dose-dependent.High concentration of baicalin could significantly promote the apoptosis of glioma cells(P<0.01).Conclusion:Baicalin can inhibit the proliferation and migration of human glioma U251 cells,and promote apoptosis,and the inhibition and promotion effects are positively correlated with the dose.Baicalin plays an important role in the study of tumor treatment effect and is expected to be a candidate drug for effective inhibition of tumor occurrence.
作者 郑寿招 党源 ZHENG Shouzhao;DANG Yuan(Department of Clinical Laboratory,Gutian Hospital,Gutian County,Fujian Province 352200;不详)
出处 《医学理论与实践》 2023年第19期3244-3247,3243,共5页 The Journal of Medical Theory and Practice
关键词 黄芩苷 神经胶质瘤 增殖 凋亡 Baicalin Glioma Proliferate Apoptosis
  • 相关文献

参考文献2

二级参考文献4

共引文献29

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部