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Emulsified Isoflurane Preconditioning Protects Isolated Rat Kupffer Cells against Hypoxia/Reoxygenation-Induced Injury

机译:乳化异氟烷预处理可保护离体大鼠Kupffer细胞免受缺氧/复氧诱导的损伤

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摘要

>Objective: To investigate the protective effect of emulsified isoflurane (EI) preconditioning on isolated rat Kupffer cells (KCs) subjected to hypoxia/reoxygenation (H/R)-induced injury.>Materials and methods: KCs were isolated by collagenase digestion and purified by Percoll density gradient centrifugation. Primary cultured KCs were divided into five groups: control, H/R plus 0.1% lipid preconditioning, and H/R plus 0.05%, 0.1% or 0.2% emulsified isoflurane preconditioning groups. H/R was induced by 4 h of hypoxia followed by 6 h of reoxygenation. Reactive oxygen species (ROS) production in the KCs and the concentration of tumor necrosis factor-α (TNF-α) in the KC culture media were measured, and the apoptosis of KCs was assayed concomitantly.>Results: ROS and TNF-α production were markedly induced in the H/R + lipid group, and lower in the 0.2% and 0.1% EI groups (P<0.05). The apoptotic rate in the H/R + lipid group was significantly higher than that in the 0.2% and 0.1% EI groups (P<0.05).>Conclusions: Emulsified isoflurane protects isolated rat KCs against H/R induced injury by decreasing the production of ROS and TNF-α and attenuating apoptosis in KCs.
机译:>目的:研究乳化异氟烷(EI)预处理对缺氧/复氧(H / R)诱导的大鼠分离Kupffer细胞(KC)的保护作用。>材料和方法: 通过胶原酶消化分离KCs,并通过Percoll密度梯度离心法纯化。原代培养的KC分为5组:对照组,H / R加0.1%的脂质预处理和H / R加0.05%,0.1%或0.2%的乳化异氟烷预处理组。 H / R由缺氧4 h,然后再充氧6 h诱导。测量KCs中活性氧(ROS)的产生和KC培养基中肿瘤坏死因子-α(TNF-α)的浓度,并同时检测KCs的凋亡。>结果: H / R +脂质组显着诱导ROS和TNF-α产生,而EI组在0.2%和0.1%时显着降低(P <0.05)。 H / R +脂质组的细胞凋亡率显着高于0.2%和0.1%EI组的细胞凋亡率(P <0.05)。>结论:乳化异氟烷可保护离体大鼠KCs免受H / R的侵害通过降低ROS和TNF-α的产生并减弱KCs的细胞凋亡来诱导损伤。

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