PI3K/AKT/mTOR通路
细胞周期蛋白D1
蛋白激酶B
化学
没食子酸
免疫组织化学
细胞生长
癌症研究
细胞周期
增生
信号转导
药理学
内分泌学
生物
内科学
细胞
医学
生物化学
抗氧化剂
作者
Caijie Zheng,Yi Wang,Beilei Bi,Wencheng Zhou,Xinran Cao,Chenyang Zhang,Wentian Lu,Yang Sun,Jiao Qu,Wen Lv
标识
DOI:10.1016/j.jphs.2024.02.015
摘要
Gallic acid (GA) is an organic compound with phenolic properties that occurs naturally and can be found in Guizhi Fuling capsules, showcasing a wide range of biological functionalities. The objective of this study was to examine the influence of GA on endometrial hyperplasia (EH) and elucidate its underlying mechanism. Initially, the induction of EH was achieved by administering estradiol to mice via continuous subcutaneous injection for a duration of 21 days. Concurrently, GA treatment was administered, and subsequently, the uterine tissue structure was assessed using hematoxylin and eosin (H&E) staining. Following this, the proliferation of human endometrial cells treated by GA was determined utilizing the CCK-8 method. Furthermore, network pharmacology and single-cell-RNA-seq data were employed to identify the target of GA action. In addition, we will employ immunofluorescence (IF), immunohistochemistry (IHC), flow cytometry and RT-qPCR methodologies to investigate the impact of GA on the expression level of cyclin D1, PI3K, p-PI3K, AKT, p-AKT. GA treatment ameliorated histopathological alterations in the uterus and suppress proliferation. Estradiol stimulation can activate the PI3K/AKT pathway, leading to up-regulation of cyclin D1 expression, whereas GA treatment results in down-regulation of its expression. The expression of cyclin D1 is down-regulated by GA through the inhibition of the PI3K/AKT pathway, effectively mitigating estradiol-induced EH in mice.
科研通智能强力驱动
Strongly Powered by AbleSci AI