Fujian Institute of Hematology, Fujian Provincial Key Laboratory of Hematology, Fujian Medical University Union Hospital, 29 Xinquan Road, Fuzhou, 350000 Fujian, China.
J Exp Clin Cancer Res. 2012 May 20;31(1):48. doi: 10.1186/1756-9966-31-48.
Baicalin, a flavone present in Scutellaria baicalensis Georgi, inhibits the growth of human leukemia and myeloma cells through induction of apoptosis.
The present study was undertaken to ascertain whether cultured Burkitt lymphoma cells undergo apoptosis when treated with baicalin. Growth rates were measured using MTT and colony formation assays, and induction of apoptosis was quantified using Annexin V and DNA fragmentation assays. Mechanisms underlying observed growth suppression were examined using Western blotting.
Treatment of CA46 Burkitt lymphoma cells with baicalin for 48 h markedly decreased the rate of cell proliferation; an IC50 value of 10 μM was obtained. Colony formation was almost fully suppressed at 10 μM baicalin. CA46 cells underwent apoptosis in response to baicalin treatment as evidenced by an increase in the percentage of cells stainable with Annexin V, by increased DNA fragmentation, and by activation of the intrinsic (mitochondrial) pathway for cell death as characterized by increased expression of the cleaved forms of caspase-9, caspase-3, and poly (ADP-ribose) polymerase. Additionally, baicalin was found to down-regulate anti-apoptotic and up-regulate apoptotic components of the phosphatidylinositide-3-kinase (PI3K)/serine/threonine kinase (Akt) signaling pathway.
The concentrations at which baicalin altered expression of components of the PI3K/Akt pathway in CA46 cells were comparable to those that suppressed growth and induced apoptosis, supporting the hypothesis that the observed growth-inhibitory and apoptosis-inducing actions of baicalin in these cells are mediated by down-regulation of this pathway.
黄芩苷是黄芩中的一种黄酮类化合物，可通过诱导细胞凋亡抑制人白血病和骨髓瘤细胞的生长。
本研究旨在确定黄芩苷处理培养的伯基特淋巴瘤细胞是否会发生细胞凋亡。使用 MTT 和集落形成测定法测量生长速率，并使用 Annexin V 和 DNA 片段化测定法定量诱导细胞凋亡。使用 Western blot 检查观察到的生长抑制的潜在机制。
黄芩苷处理 CA46 伯基特淋巴瘤细胞 48 小时后，明显降低细胞增殖率；IC50 值为 10 μM。在 10 μM 黄芩苷下，集落形成几乎完全受到抑制。CA46 细胞在黄芩苷处理下发生凋亡，这表现在 Annexin V 染色细胞百分比增加、DNA 片段化增加以及细胞死亡的内在（线粒体）途径激活，特征是 cleaved 形式的 caspase-9、caspase-3 和聚（ADP-核糖）聚合酶表达增加。此外，发现黄芩苷下调抗凋亡并上调磷脂酰肌醇 3-激酶（PI3K）/丝氨酸/苏氨酸激酶（Akt）信号通路的凋亡成分。
黄芩苷改变 CA46 细胞中 PI3K/Akt 通路成分表达的浓度与抑制生长和诱导凋亡的浓度相当，支持以下假说：即黄芩苷在这些细胞中观察到的生长抑制和凋亡诱导作用是通过下调该途径介导的。
