论文部分内容阅读
研究了双酚A(BPA)对肝癌细胞HepG2增殖的影响及其分子机制。通过MTT实验发现,在环境浓度BPA(1×10-8 mol/L)暴露下,人肝癌HepG2细胞增殖显著升高[(156±2.48)%]。Western blotting和实时定量PCR结果显示,环境浓度的BPA处理HepG2细胞24h,细胞中NF-κB以及其下游相关炎症因子IL-1β、TNF-α的转录均明显上调。免疫荧光染色结果显示,BPA处理导致HepG2细胞内ROS显著上升;而ROS抑制剂NAC及雌激素受体抑制剂ICI 182 780均可有效抑制由BPA引起的细胞增殖和胞内p65上升。研究结果表明,BPA通过激活HepG2细胞中的雌激素受体诱导了细胞ROS的产生,随后引起细胞内炎症因子表达上调,促进细胞增殖。
The effects of bisphenol A (BPA) on the proliferation of hepatoma HepG2 cells and its molecular mechanism were studied. MTT assay showed that under the exposure of environmental BPA (1 × 10-8 mol / L), the proliferation of HepG2 cells was significantly increased [(156 ± 2.48)%]. The results of Western blotting and real-time PCR showed that the transcription of NF-κB, IL-1β and TNF-α in HepG2 cells treated with BPA at ambient concentration was significantly up-regulated. Immunofluorescence staining showed that BPA treatment resulted in a significant increase of ROS in HepG2 cells; while NAC, an inhibitor of ROS, and ICI 182 780, an inhibitor of estrogen receptor, inhibited BPA-induced cell proliferation and intracellular increase of p65. The results show that BPA induces the production of ROS by activating the estrogen receptor in HepG2 cells, and then induces the up-regulation of intracellular inflammatory cytokines and cell proliferation.