Zheng C M, Liu X Z, Li Q L, Wang J F, Tan Z, Ge M H
Department of Head and Neck Surgery, Zhejiang Cancer Hospital, Hangzhou 310022, China.
Biospecimen Repository, Zhejiang Cancer Hospital, Hangzhou 310022, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2017 Jun 7;52(6):458-462. doi: 10.3760/cma.j.issn.1673-0860.2017.06.012.
To investigate the effect of icariin (ICA) on the bisphenol A (BPA)-enhanced proliferation function of thyroid carcinoma cell B-CPAP and underlying mechanism. The proliferation of Gastric B-CPAP cell line was evaluated by cell counting kit-8 (CCK-8). Apoptosis and ROS expression in B-CPAP cells were detected by flow cytometry. The expression of superoxide dismutase (SOD) and malondialdehyde (MDA) in B-CPAP cells were measured by individual assay kits. The expressions of Bcl-2 and γ-HA2X were detected by Western blot. SPSS 18.0 software was used to analyze the data. B-CPAP cell activity was promoted by treatment with 3×10(-7)mol/L BPA for 48 h, with significant difference in absorbance between BPA and control groups (1.089±0.053 0.935±0.010, <0.05). The cell activities of BPA+ ICA(25), BPA+ ICA(50), BPA+ ICA(100) and BPA+ ICA(200) groups was 0.780±0.036, 1.007±0.050, 0.958±0.033 and 0.625±0.064, respectively (all <0.01). The proliferation of B-CPAP cells treated with BPA for 72 hours showed a similar trend to 48 hours. There was no significant difference between all treatment groups in 24 hours. The apoptosis rate was (19.272±0.186)% in BPA-treated cells, and was (22.412±0.238)% in control cells (<0.05). The apoptosis rates of BPA+ ICA(50) and BPA+ ICA(200) groups were (23.688±0.412)% and (30.270±0.696)%, respectively (<0.01). The intracellular accumulation of ROS in BPA, BPA+ ICA(50), and BPA+ ICA(200) groups were 806±21, 1 772±37, 2 041±16, respectively (<0.01). The expressions of anti-apoptotic protein Bcl-2 in control, BPA, BPA+ ICA(50), BPA+ ICA(200) groups were 7 120±151, 9 801±286, 5 902±171 and 4 203±216, respectively (<0.01). BPA can promote the proliferation of thyroid carcinoma B-CPAP cells and decrease the apoptosis of cells, and this effect can be inhibited by ICA. The possible mechanism is to induce high expression of intracellular ROS and inhibit the expression of antioxidase system, leading to cell oxidative damage, thereby inducing apoptosis.
探讨淫羊藿苷（ICA）对双酚A（BPA）增强甲状腺癌细胞B-CPAP增殖功能的影响及其潜在机制。采用细胞计数试剂盒-8（CCK-8）评估胃B-CPAP细胞系的增殖情况。通过流式细胞术检测B-CPAP细胞中的凋亡和活性氧（ROS）表达。使用单独的检测试剂盒测定B-CPAP细胞中超氧化物歧化酶（SOD）和丙二醛（MDA）的表达。通过蛋白质免疫印迹法检测Bcl-2和γ-H2AX的表达。使用SPSS 18.0软件分析数据。用3×10（-7）mol/L BPA处理48小时可促进B-CPAP细胞活性，BPA组与对照组的吸光度有显著差异（1.089±0.053对0.935±0.010，P<0.05）。BPA+ICA（25）、BPA+ICA（50）、BPA+ICA（100）和BPA+ICA（200）组的细胞活性分别为0.780±0.036、1.007±0.050、0.958±0.033和0.625±0.064（均P<0.01）。用BPA处理72小时的B-CPAP细胞增殖情况与48小时相似。所有处理组在24小时时无显著差异。BPA处理的细胞凋亡率为（19.272±0.186）%，对照组为（2
