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Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type Ⅱalveolar epithelial cells

机译:依达拉奉通过抑制人Ⅱ型肺泡上皮细胞的氧化应激减轻百草枯引起的肺损伤

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BACKGROUND:Edaravone(3-methyl-1-penyl-2-pyrazolin-5-one) is a potent free-radical scavenger and has the antioxidant ability to inhibit lipid peroxidation.The study aimed to examine the effect of edaravone on protecting the acute injury of human type II alveolar epithelial cells(A549cells) induced by paraquat(PQ) and the change of production of reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD).METHODS:A549 cells were cultured and divided into PQ group(group P),edaravone-treated group(group E) and normal control group(group C).The cells in group P were exposed to paraquat(600 umol/L),and the cells in group E were treated with edaravone(100 umol/L) additionally,and no drug intervention was given to the cells in group C.Real-time monitoring by LSCM was used to detect the cell response and the intracellular dynamic change of ROS level in A549 cells after administration of PQ and edaravone.And the levels of SOD and MDA were detected respectively by biochemistry colorimetry.Data were expressed as mean ± standard error of the mean.Statistical analysis was carried out with the soft SPSS 16.0.RESULTS:The concentration of intracellular ROS significantly increased when PQ was given to A549 cells.But after administration of edaravone,the concentration of intracellular ROS was decreased.Compared to the PQ group,the levels of SOD in the edaravone group were significantly increased while the levels of MDA were markedly decreased.CONCLUSIONS:Paraquat can increase the oxidative stress,and induce the lipid peroxidation of A549 cells.Edaravone has the effect to scavenge reactive oxygen species,and to protect against the PQ-induced lung toxicity.
机译:背景:依达拉奉(3-甲基-1-苯基-2-吡唑啉-5-酮)是一种强力的自由基清除剂,具有抗脂质过氧化的抗氧化能力。本研究旨在探讨依达拉奉对急性心肌损伤的保护作用。百草枯(PQ)对人II型肺泡上皮细胞(A549细胞)的损伤及活性氧(ROS),丙二醛(MDA),超氧化物歧化酶(SOD)的产生变化。将METHODS:A549细胞培养并分为PQ组(P组),依达拉奉治疗组(E组)和正常对照组(C组)。P组细胞暴露于百草枯(600 umol / L),E组细胞经依达拉奉处理(100 umol / L),且未对C组细胞进行药物干预。采用LSCM实时监测法检测PQ和PQ后A549细胞的细胞应答和ROS水平的细胞内动态变化。依达拉奉。生化比色法分别检测SOD和MDA水平数据以平均值±平均值的标准误表示。用软件SPSS 16.0进行统计分析。结果:P549给予A549细胞后,细胞内ROS的浓度显着增加。与PQ组相比,依达拉奉组的SOD水平明显升高,而MDA水平明显降低。结论:百草枯能增加氧化应激,诱导A549细胞脂质过氧化。依达拉奉具有清除活性氧的作用,并防止PQ诱导的肺毒性。

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