PI3K/AKT/mTOR通路
蛋白激酶B
血管生成
活力测定
西罗莫司
细胞生物学
药理学
内皮干细胞
脐静脉
细胞凋亡
伤口愈合
癌症研究
磷酸化
化学
医学
生物
信号转导
免疫学
内科学
生物化学
体外
作者
Min Zhang,Rongrong Zhu,Libin Zhang
出处
期刊:Chemosphere
[Elsevier]
日期:2020-02-01
卷期号:241: 125077-125077
被引量:27
标识
DOI:10.1016/j.chemosphere.2019.125077
摘要
Triclosan (TCS) has potentially toxic effects on humans and animals. However, the possible roles and mechanisms of TCS in endothelial cells (ECs) are still unknown. Abnormal damage to ECs and vascular function is a critical process in various cardiovascular diseases, including coronary artery disease (CAD), atherosclerosis, stroke, and hypertension. Hence, we explored the potential toxicological roles of TCS in EC functions. Cell Counting Kit-8, apoptosis, transwell, wound healing, and tube-formation experiments were performed to evaluate the effects of TCS on human umbilical vein endothelial cell (HUVEC) function. Additionally, the levels of PI3K, Akt, and mTOR phosphorylation were measured by Western blot. The results indicated that TCS treatment suppressed HUVECs viability, migration and angiogenesis. TCS treatment increased the expression of inflammatory markers and ROS in cultured HUVECs. Moreover, TCS treatment inhibited PI3K/Akt/mTOR expression. All of these results reveal that TCS induces notable vascular injury and affects the viability, migration and angiogenic capacity of HUVECs, at least in part via the PI3K/Akt/mTOR signaling pathway.
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