ArticlePsychopharmacology2016
Lithium ions attenuate serum-deprivation-induced apoptosis in PC12 cells through regulation of the Akt/FoxO1 signaling pathways.
Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Traditional Chinese Medicine-derived formulations and extracts modulating the PI3K/AKT pathway in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Comparison of Chemical Compositions and Antioxidant Activity of Essential Oils from Litsea Cubeba, Cinnamon, Anise, and Eucalyptus.Molecules (Basel, Switzerland) · 2023Article
- Hydroxysafflor Yellow A and Anhydrosafflor Yellow B Protect Against Cerebral Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and ApoptosisFrontiers in pharmacology · 2021Article
- Effects of lithium on the secretory production of recombinant antibody from insect cells.In vitro cellular & developmental biology. Animal · 2019Article
- Statins induce cell apoptosis through a modulation of AKT/FOXO1 pathway in prostate cancer cells.Cancer management and research · 2019Article
- HOncotarget · 2017Article
- Treatment of Bipolar Disorder in a Lifetime Perspective: Is Lithium Still the Best Choice?Clinical drug investigation · 2017Review
- Artemisinin protects PC12 cells against β-amyloid-induced apoptosis through activation of the ERK1/2 signaling pathway.Redox biology · 2017Article
- αMSH prevents ROS-induced apoptosis by inhibiting Foxo1/mTORC2 in mice adipose tissue.Oncotarget · 2017Article
- Effect of lithium on ventricular remodelling in infarcted rats via the Akt/mTOR signalling pathways.Bioscience reports · 2017Article
- Palmitic acid triggers cell apoptosis in RGC-5 retinal ganglion cells through the Akt/FoxO1 signaling pathway.Metabolic brain disease · 2017Article
- Nerve growth factor protects against palmitic acid-induced injury in retinal ganglion cells.Neural regeneration research · 2016Article
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleLithium is currently used in the treatment of mental illness. We have previously reported that lithium stimulated the protein kinase B/Forkhead box O1 (Akt/FoxO1) pathway in rats. However, little information is available regarding its neuroprotective role of this pathway and underlying mechanisms.
objectivesPC12 cells treated with serum deprivation were used as a toxicity model to study the protective effect of lithium and its underlying mechanisms.
methodsCell viability was determined by methyl thiazolyl tetrazolium assay and Hoechst staining. FoxO1 subcellular location and its overexpression were used to study the underlying mechanisms. Various pathway inhibitors were used to investigate the possible pathways, while the phosphorylation of Akt and FoxO1 was analyzed by Western blot.
resultsLithium pretreatment dose-dependently reduced PC12 cell apoptosis induced by serum starvation. The protective effect of lithium was abolished by LY294002, a PI3K-specific inhibitor, and Akt inhibitor Akt inhibitor VIII, whereas mitogen-activated protein kinase kinase (MEK kinase) inhibitor U0126 had no effect. Lithium induced the phosphorylation of Akt and FoxO1 in a time- and concentration-dependent manner. Lithium-induced phosphorylation of Akt and FoxO1 is mediated by the PI3K/Akt pathway. Serum deprivation caused nuclear translocation of FoxO1 while application of lithium reversed the effect of serum deprivation. Moreover, overexpression of FoxO1 enhanced cell apoptosis induced by serum withdrawal. Finally, lithium was found to reduce the exogenous and endogenous FoxO1 protein levels in PC12 cells in a concentration-dependent fashion.
conclusionsThe protective effect of lithium against serum starvation cell death is mediated by the PI3K/Akt/FoxO1 pathway.
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