高浓度碘普罗胺诱导人胚肾细胞凋亡和自噬，激活 ROS 依赖的细胞应激途径。
High Concentration of Iopromide Induces Apoptosis and Autophagy in Human Embryonic Kidney Cells Activating a ROS-dependent Cellular Stress Pathway.
机构信息
Department of Diagnostic Radiology, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan, R.O.C.
School of Medicine, Fu-Jen Catholic University, New Taipei, Taiwan, R.O.C.
出版信息
In Vivo. 2021 Nov-Dec;35(6):3221-3232. doi: 10.21873/invivo.12617.
BACKGROUND/AIM: The use of iodinated contrast media may impair renal function. However, no report has addressed the nephrotoxicity of high doses of iodinated contrast media in normal kidney cells and its associated molecular mechanisms.
MATERIALS AND METHODS
Cell proliferation was assessed using the MTT assay. Cell death was evaluated through examining the morphological changes and TUNEL assay. Autophagy was detected through acridine orange staining and lysotracker staining. Reactive oxygen species production and AKT kinase activity were examined.
RESULTS
Iopromide induced cell death and triggered apoptosis and autophagy in HEK 293 cells. Cell viability was significantly restored in the presence of a pan-caspase inhibitor or a ROS scavenger, N-acetyl-L-cysteine. AKT kinase activity was found to be reduced in iopromide-treated HEK 293 cells.
CONCLUSION
High concentrations of iopromide induce cell damage, apoptosis, and autophagy through down-regulating AKT and ROS-activated cellular stress pathways in HEK 293 cells.
背景/目的：碘造影剂的使用可能会损害肾功能。然而，目前尚无报道涉及高剂量碘造影剂在正常肾细胞中的肾毒性及其相关的分子机制。
材料和方法
通过 MTT 法评估细胞增殖。通过观察形态变化和 TUNEL 检测评估细胞死亡。通过吖啶橙染色和溶酶体追踪染色检测自噬。检测活性氧（ROS）的产生和 AKT 激酶活性。
结果
碘普罗胺诱导 HEK 293 细胞死亡，并引发细胞凋亡和自噬。在存在泛半胱天冬酶抑制剂或 ROS 清除剂 N-乙酰-L-半胱氨酸的情况下，细胞活力显著恢复。碘普罗胺处理的 HEK 293 细胞中发现 AKT 激酶活性降低。
结论
高浓度的碘普罗胺通过下调 AKT 和 ROS 激活的细胞应激途径，诱导 HEK 293 细胞损伤、凋亡和自噬。
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