大叶茜草素对宫颈癌细胞增殖、粘附及糖酵解水平的分子机 制研究
摘要
(PI3K/AKT)的调控作用。方法:体外培养人宫颈癌 HeLa 细胞,激活剂组(50 μmol/L 大叶茜草素 +10 μmol/LPI3K/
AKT 通路激活剂 SC-79)和抑制剂组(50 μmol/L 大叶茜草素+ 2 μmol/L PI3K/AKT 通路抑制剂 LY294002),干预 24 h。
采 用 5- 乙炔基 -2’脱氧尿嘧啶核苷(EdU)法、细胞粘附实验、乳酸、葡萄糖检测试剂盒、蛋白免疫印迹(WB)法进
行分 析。结果:实验组和阳性药物组细胞增殖率、粘附数、乳酸含量、葡萄糖消耗水平、己糖激酶 2(HK2)、乳酸脱氢
酶 A(LDHA)、甘油醛 -3- 磷酸脱氢酶(GAPDH)、p-PI3K、p-AKT(P<0.05)。结论:大叶茜草素作用机制可能与
抑制 PI3K/AKT 通路转导有关。
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