Baicalin is a major component of PC-SPES which inhibits the proliferation of human cancer cells via apoptosis and cell cycle arrest
Baicalin is a major component of PC-SPES which inhibits the proliferation of human cancer cells via apoptosis and cell cycle arrest
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DOI：
10.1002/pros.10024
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发表时间：
2001-12-01
期刊：
影响因子：
2.8
通讯作者：
Koeffler, HP
中科院分区：
文献类型：
--
作者：
Ikezoe, T;Chen, SS;Koeffler, HP
背景。PC-SPES是一种八种草药的混合物，被证明对前列腺癌有活性。最近，我们用高效液相色谱（HPLC）从PC-SPES中分离出黄芩苷的主要成分（占总乙醇提取物的6%）。黄芩苷对不同类型肿瘤（PC-3、DU145、LNCaP前列腺癌细胞系、MCF-7乳腺癌细胞系、HL-60成髓细胞白血病细胞系和NB4早幼粒细胞白血病细胞系）的克隆生长和细胞周期阻滞能力进行了评价。黄芩苷诱导癌细胞凋亡的能力通过Annexin V染色和检测聚（adp -核糖）聚合酶（PARP）的裂解(3)来检测。Western blot检测黄芩苷对这些细胞中p2（waf1）和p27（kip1）水平的影响。此外，通过表达cd11b来检测HL-60细胞的分化诱导作用。黄芩苷对LNCaP和PC3前列腺癌细胞以及HL-60和NB4骨髓母细胞/早幼粒细胞白血病细胞株的抑制作用为50% (ED50)，范围在6.4 × 10(-6) ~ 12 × 10(-6) mol/L之间。细胞周期分析表明，黄芩苷（2 × 10(-5) mol/L, 4 d）对LNCaP和HL-60细胞的累积量分别为G(0)/G(1)和G(2)/M。同时，通过CD11b抗原的表达、膜联蛋白V染色、PARP的切割检测，HL-60细胞被诱导分化和凋亡。黄芩苷还能增强LNCaP和HL-60细胞中周期蛋白依赖性激酶抑制剂p27（kip1）的表达。黄芩苷通过细胞凋亡和细胞周期阻滞抑制癌细胞增殖，其中p27（kip1）可能起作用。黄芩苷可能是一种新型的辅助治疗肿瘤，包括前列腺癌。(C) 2001 Wiley-Liss, Inc。
BACKGROUND. PC-SPES is an eight-herb mixture that was shown to have activity against Prostate cancer. Recently, we isolated a major component (6% of the total ethanolic extract) known as baicalin from PC-SPES by high performance liquid chromatography (HPLC).METHODS. Baicalin was evaluated for its ability to inhibit clonal growth, and to induce cell cycle arrest of various cancer types (PC-3, DU145, LNCaP prostate cancer cell lines, MCF-7 breast cancer cell line, HL-60 myeloblastic leukemia cell line, and NB4 promyelocytic leukemia cell line). The ability of baicalin to induce apoptosis of cancer cells was examined by both staining with Annexin V and detection of cleavage of Poly (ADP-ribose) polymerase (PARP)(3). Western blot analysis examined the effect of baicalin on levels of p2(waf1) and p27(kip1) in those cells. Futhermore, induction of differentiation in HL-60 cells was measured by expression of CD11b.RESULTS. Baicalin inhibited the clonal proliferation of LNCaP and PC3 prostate cancer cell lines, and the HL-60 and NB4 myeloblastic/promyelocytic leukemia cell lines with a 50% inhibition (ED50) that ranged between 6.4 x 10(-6) to 12 x 10(-6) mol/L. Cell cycle analysis showed that baicalin (2 x 10(-5) mol/L, 4 days) caused a G(0)/G(1) and G(2)/M accumulation of LNCaP and HL-60 cells, respectively. Concomitantly, differentiation and apoptosis were induced in HL-60 cells, as measured by expression of CD11b antigen, staining with annexin V, and detection of cleavage of PARP. Moreover, baicalin enhanced the expression of the cyclin-dependent kinase inhibitor, p27(kip1) in LNCaP and HL-60 cells.CONCLUSIONS. Baicalin inhibited the proliferation of cancer cells via apoptosis and cell cycle arrest, in which p27(kip1) may play a role. Baicalin may be a novel, adjunctive therapy for selected malignancies including prostate cancer. (C) 2001 Wiley-Liss, Inc.