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镉的细胞毒性及其在人滋养层细胞 HTR-8/SVneo 中的可能作用机制。

Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR-8/SVneo cells.

机构信息

College of Life Science, Sichuan Normal University, Chengdu, China.

Department of Orthopedics and Traumatology of Traditional Chinese Medicine, Sichuan 2nd Hospital of Traditional Chinese Medicine, Chengdu, China.

出版信息

Environ Toxicol. 2021 Jun;36(6):1111-1124. doi: 10.1002/tox.23110. Epub 2021 Feb 9.

Abstract

The accumulation of cadmium (Cd) in the human body through food chain can lead to adverse pregnancy outcomes. In this study, Cd cytotoxicity and its mechanisms in HTR-8/SVneo cells were investigated. Cd disrupted the cellular submicrostructure and inhibited the cell viability in a time- and dose-dependent manner. The levels of reactive oxygen species, malondialdehyde content, and the activities of glutathione peroxidase (GSH-Px) and total superoxode dismutase (T-SOD) were concentration-dependently increased by Cd. In addition, Cd dose-dependently inducedcell apoptosis and decreased cell migration and invasion capacities. Finally, Cd significantly upregulated all the genes related to oxidative stress (SOD1, ROS1, and HSPA6), inflammatory response, cell cycle, apoptosis, and migration and invasion. This study will provide insights into the prevention and treatment of pregnancy-related diseases caused by Cd intoxication.

摘要

镉(Cd)在人体内通过食物链的积累可能会导致不良的妊娠结局。在这项研究中,研究了 Cd 对 HTR-8/SVneo 细胞的细胞毒性及其作用机制。Cd 以时间和剂量依赖的方式破坏细胞亚微观结构并抑制细胞活力。Cd 浓度依赖性地增加了活性氧(ROS)水平、丙二醛含量以及谷胱甘肽过氧化物酶(GSH-Px)和总超氧化物歧化酶(T-SOD)的活性。此外,Cd 剂量依赖性地诱导细胞凋亡并降低细胞迁移和侵袭能力。最后,Cd 显著上调了与氧化应激(SOD1、ROS1 和 HSPA6)、炎症反应、细胞周期、凋亡以及迁移和侵袭相关的所有基因。本研究将为预防和治疗由 Cd 中毒引起的与妊娠相关的疾病提供新的思路。

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