ArticleJournal of molecular neuroscience : MN2013
Neuroprotective effect of leukemia inhibitory factor on antimycin A-induced oxidative injury in differentiated PC12 cells.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Modulatory Effect of Myokines on Reactive Oxygen Species in Ischemia/Reperfusion.International journal of molecular sciences · 2020Review
- IL-5 blocks apoptosis and tau hyperphosphorylation induced by AβJournal of physiology and biochemistry · 2017Article
- Triptolide Inhibited Cytotoxicity of Differentiated PC12 Cells Induced by Amyloid-Beta₂₅₋₃₅ via the Autophagy Pathway.PloS one · 2015Article
- Identification of a novel neurotrophic factor from primary retinal Müller cells using stable isotope labeling by amino acids in cell culture (SILAC).Molecular & cellular proteomics : MCP · 2014Article
- Neuroprotective effect of CNB-001, a novel pyrazole derivative of curcumin on biochemical and apoptotic markers against rotenone-induced SK-N-SH cellular model of Parkinson's disease.Journal of molecular neuroscience : MN · 2013Article
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4 authors at 1 institution in 1 country.
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Abstract
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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