College of Medicine, Nankai University, Tianjin, 300071, China.
J Mol Neurosci. 2013 Jul;50(3):577-85. doi: 10.1007/s12031-013-0004-x. Epub 2013 May 1.
As a neurotrophic cytokine, leukemia inhibitory factor (LIF) has neuroendocrine effects and exerts neuroprotective effects on various neuron injuries both in vitro and in vivo. The aim of the present study was to investigate whether LIF can protect PC12 cells from antimycin A (AMA)-induced oxidative stress. LIF (0.5 and 1 ng/ml) increased PC12 cell viability and significantly attenuated AMA-induced cell death as demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Results from Hoechst 33342 staining and flow cytometry assay showed that AMA induced apoptosis significantly in PC12 cells, while pretreatment with LIF (0.5 and 1 ng/ml) can attenuate this injury. The presence of LIF partly prevented AMA-induced elevated reactive oxygen species level and decreased superoxide dismutase level, which indicated the antioxidative effects of LIF on the neuron oxidative injury. In conclusion, LIF might protect PC12 cells from the injury induced by AMA through the downregulation of oxidative stress, which may provide basic information of using LIF as a potential targeted therapy for oxidative injury in neurons.
作为一种神经营养细胞因子，白血病抑制因子（LIF）具有神经内分泌作用，并在体外和体内对各种神经元损伤发挥神经保护作用。本研究旨在探讨 LIF 是否可以保护 PC12 细胞免受抗霉素 A（AMA）诱导的氧化应激。LIF（0.5 和 1ng/ml）增加了 PC12 细胞活力，并通过 3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴化物测定法显著减轻了 AMA 诱导的细胞死亡。Hoechst 33342 染色和流式细胞术检测结果表明，AMA 可显著诱导 PC12 细胞凋亡，而 LIF（0.5 和 1ng/ml）预处理可减轻这种损伤。LIF 的存在部分阻止了 AMA 诱导的活性氧水平升高和超氧化物歧化酶水平降低，这表明 LIF 对神经元氧化损伤具有抗氧化作用。总之，LIF 可能通过下调氧化应激来保护 PC12 细胞免受 AMA 诱导的损伤，这可为将 LIF 作为神经元氧化损伤的潜在靶向治疗提供基础信息。
