Han Se Eun, Park Chan Ho, Nam-Goong Il Sung, Kim Young Il, Kim Eun Sook
Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea.
Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea
In Vivo. 2019 Mar-Apr;33(2):375-382. doi: 10.21873/invivo.11484.
BACKGROUND/AIM: The aim of the study was to evaluate the anticancer effects of baicalein in FRO anaplastic thyroid cancer (ATC) cells.
FRO cells were treated with baicalein and viability was measured by the MTT assay. Cell apoptosis was observed by staining with Hoechst dye. The expression of apoptotic proteins (Bax, Bcl-2, PARP, cytochrome c, and caspase-3) and the inflammatory protein Cox-2 and the phosphorylation of MAPKs and Akt were determined by western blot.
Treatment with baicalein inhibited cell proliferation in a time-dependent manner and increased DNA fragmentation and apoptosis in FRO cells. Baicalein at 50 and 100 μM inhibited the expression of Bax, PARP, cytochrome c, cleaved caspase-3, and Cox-2, and increased the expression of Bcl-2. Baicalein increased the phosphorylation of ERK, p38 MAPK, and Akt and decreased JNK phosphorylation.
Baicalein caused anticancer effects in FRO ATC cells through induction of apoptosis and regulation of the MAPK and Akt pathway.
背景/目的：本研究旨在评估黄芩素对FRO间变性甲状腺癌（ATC）细胞的抗癌作用。
用黄芩素处理FRO细胞，通过MTT法检测细胞活力。用Hoechst染料染色观察细胞凋亡。通过蛋白质免疫印迹法测定凋亡蛋白（Bax、Bcl-2、PARP、细胞色素c和半胱天冬酶-3）、炎性蛋白Cox-2的表达以及丝裂原活化蛋白激酶（MAPKs）和Akt的磷酸化水平。
黄芩素处理以时间依赖性方式抑制细胞增殖，并增加FRO细胞中的DNA片段化和细胞凋亡。50和100μM的黄芩素抑制Bax、PARP、细胞色素c、裂解的半胱天冬酶-3和Cox-2的表达，并增加Bcl-2的表达。黄芩素增加细胞外信号调节激酶（ERK）、p38丝裂原活化蛋白激酶和Akt的磷酸化水平，并降低应激活化蛋白激酶（JNK）的磷酸化水平。
黄芩素通过诱导细胞凋亡以及调节MAPK和Akt信号通路对FRO ATC细胞产生抗癌作用。
