Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 50, Issue 3, Pages 577-585Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-013-0004-x
Keywords
Leukemia Inhibitory Factor; Antimycin A; PC12 cells; Apoptosis; Reactive oxygen species; Superoxide dismutase
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Funding
- Tianjin Research Program of Application Foundation and Advanced Technology [10JCZDJC19100]
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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.
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