Effect of Icaritin on K562 Cell Proliferation and Intracellular Reactive Oxygen Species / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To investigate the effect of icaritin (ICT) on proliferation of K562 cells and reactive oxygen species (ROS) in patients with chronic myeloid leukemia (CML).</p><p><b>METHODS</b>MTT assay was used to detect the effect of ICT on the proliferation of K562 cells. Flow cytometry was used to detect the apoptosis of K562 cells and intracellular ROS level. The expression of PARP protein was detected by Western blot.</p><p><b>RESULTS</b>ICT obviously inhibited the proliferation of K562 cells and induced their apoptosis, the expression of PARP protein was enhanced, and the intracellular ROS increased significantly.</p><p><b>CONCLUSION</b>The ICT showes the inhibitory effects on proliferation and apoptosis-inducing effects on K562 cells, and thier mechanism relats with the increase of reactive oxygen species in the cells.</p>

High levels of testosterone inhibit ovarian follicle development by repressing the FSH signaling pathway / 华中科技大学学报（医学）（英德文版）

The effect of high concentrations of testosterone on ovarian follicle development was investigated. Primary follicles and granulosa cells were cultured in vitro in media supplemented with a testosterone concentration gradient. The combined effects of testosterone and follicle-stimulating hormone (FSH) on follicular growth and granulosa cell gonadotropin receptor mRNA expression were also investigated. Follicle growth in the presence of high testosterone concentrations was promoted at early stages (days 1-7), but inhibited at later stage (days 7-14) of in vitro culture. Interestingly, testosterone-induced follicle development arrest was rescued by treatment with high concentrations of FSH (400 mIU/mL). In addition, in cultured granulosa cells, high testosterone concentrations induced cell proliferation, and increased the mRNA expression level of FSH receptor (FSHR), and luteinized hormone/choriogonadotropin receptor. It was concluded that high concentrations of testosterone inhibited follicle development, most likely through regulation of the FSH signaling pathway, although independently from FSHR downregulation. These findings are an important step in further understanding the pathogenesis of polycystic ovary syndrome.