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Microcystin-LR induced oxidative stress, inflammation, and apoptosis in alveolar type II epithelial cells of ICR mice in vitro.

微囊藻毒素-LR 在体外诱导 ICR 小鼠肺泡 ⅱ 型上皮细胞的氧化应激、炎症和凋亡。

  • 影响因子:2.45
  • DOI:10.1016/j.toxicon.2019.12.152
  • 作者列表:"Zhong S","Liu Y","Wang F","Wu Z","Zhao S
  • 发表时间:2020-01-30
Abstract

:Previous studies have shown that microcystin-LR (MC-LR) produced by toxic cyanobacterial blooms could inflict damage to the lung. However, the mechanisms underlying MC-induced pulmonary toxicity are not fully described. In this study, the primary' fetal alveolar type II epithelial cells (AEC II) from ICR mice, which are involved in formation of bioactive component of pulmonary epithelium and secretion of pulmonary surfactants, were exposed to MC-LR at different concentrations (0, 0.625, 1.25, 2.5, 5, 10, 20 μg/mL) for different time (12, 24, 36 h). Results showed that the viabilities of AEC II exposed to 10 and 20 μg MC-LR/mL were significantly decreased compared with the control group. Furthermore, MC-LR exposure resulted in overproduction of reactive oxygen species (ROS) and induced a significant reduction in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Expressions of apoptosis-related proteins including bax, cyt-c, and caspase-9 were significantly up-regulated by exposure to 2.5, 5, 10, or 20 μg MC-LR/mL. When exposed to 5, 10, or 20 μg MC-LR/mL, expressions of proteins involved in inflammatory, p-65 and iNOS were significantly greater than those of the controls. In conclusion, inflammation and apoptosis might be responsible for MC-LR-induced pulmonary injury.

摘要

: 以前的研究表明,有毒蓝藻水华产生的微囊藻毒素-LR (MC-LR) 会对肺造成损伤。然而,MC 诱导肺毒性的机制尚未完全描述。本研究主要从 ICR 小鼠的胎儿肺泡 ⅱ 型上皮细胞 (AEC ⅱ) 中筛选出参与肺上皮生物活性成分形成和分泌肺表面活性剂的细胞, 暴露于不同浓度 (0 、 0.625 、 1.25 、 2.5 、 5 、 10 、 20 μ g/mL) 的 MC-LR对于不同的时间 (12 、 24 、 36 h)。结果表明,与对照组相比,10 和 20 μ g MC-LR/mL 染毒组 AEC ⅱ 的活力显著降低。此外,MC-LR 暴露导致活性氧 (ROS) 过量产生,并诱导超氧化物歧化酶 (SOD) 和谷胱甘肽过氧化物酶 (GSH-Px) 显著降低。2.5 、 5 、 10 或 20 μ g MC-LR/mL 可显著上调细胞凋亡相关蛋白 bax 、 cyt-c 和 caspase-9 的表达。当暴露于 5 、 10 或 20 μ g MC-LR/mL 时,参与炎症、 p-65 和 iNOS 的蛋白表达显著高于对照组。总之,炎症和细胞凋亡可能是 MC-LR 诱导的肺损伤的原因。

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