ArticleNeurochemical research2016
Apelin-13 Protects PC12 Cells from Corticosterone-Induced Apoptosis Through PI3K and ERKs Activation.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
- Immunological characterization of stroke-heart syndrome and identification of inflammatory therapeutic targets.Frontiers in immunology · 2023Article
- Review
- Apelin-13 attenuates early brain injury through inhibiting inflammation and apoptosis in rats after experimental subarachnoid hemorrhage.Molecular biology reports · 2022Article
- The Neuroprotective Effect of Shenmai Injection on Oxidative Stress Injury in PC12 Cells Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Anti-Apoptotic Effect of Apelin in Human Placenta: Studies on BeWo Cells and Villous Explants from Third-Trimester Human Pregnancy.International journal of molecular sciences · 2021Article
- Fc-Elabela fusion protein attenuates lipopolysaccharide-induced kidney injury in mice.Bioscience reports · 2020Article
- Protective Effects of Ursolic Acid Against Cytotoxicity Induced by Corticosterone: Role of Protein Kinases.Neurochemical research · 2019Article
- Apelin-13 Protects PC12 Cells Against Methamphetamine-Induced Oxidative Stress, Autophagy and Apoptosis.Neurochemical research · 2019Article
- Protective effects of ethyl gallate on HMetabolic brain disease · 2019Article
- Iron Metabolism of the Skeletal Muscle and Neurodegeneration.Frontiers in neuroscience · 2019Review
- Modulation of ERK1/2 and Akt Pathways Involved in the Neurotrophic Action of Caffeic Acid Alkyl Esters.Molecules (Basel, Switzerland) · 2018Article
- Fc-apelin fusion protein attenuates lipopolysaccharide-induced liver injury in mice.Scientific reports · 2018Article
- Apelinergic System Structure and Function.Comprehensive Physiology · 2017Review
- Glycyrrhetinic acid protects H9c2 cells from oxygen glucose deprivation-induced injury through the PI3K/AKt signaling pathway.Journal of natural medicines · 2017Article
- Temporal Expression of Apelin/Apelin Receptor in Ischemic Stroke and its Therapeutic Potential.Frontiers in molecular neuroscience · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely accepted that environmental stress is a risk factor for mental disorders. Glucocorticoid hormones play a vital role in the regulation of physiological response to stress. High concentrations of corticosterone can induce cellular damage in PC12 cells, which possess typical neuronal features. Apelin and its receptor APJ are widely distributed in the central nervous system including limbic structures involved in stress responses. Previous studies have suggested that apelin has a neuroprotective function. However, the effect of apelin on corticosterone-induced neuronal damage remains to be elucidated. In the present study, we explored the potential protective activity of apelin-13 in PC12 cells treated with corticosterone and its underling mechanisms. The viability of the cells, the apoptosis of the cells, the level of phosphorylation of Akt (p-Akt) and extracellular signal-regulated kinases (p-ERKs) and cleaved caspase-3 expression were detected by MTT, Hoechst staining and flow cytometer assays and Western blotting. Results showed that corticosterone induced cells viability loss, cell apoptosis, down-regulation of p-Akt and p-ERKs and up-regulation of cleaved caspase-3. The effects induced by corticosterone were attenuated by apelin-13 pretreatment. Furthermore, apelin-13-mediated anti-viability loss, antiapoptosis and caspase-3 suppression activities were blocked by specific inhibitors of phosphatidylinositol 3-kinase (PI3K) (LY294002) and ERKs (PD98059). The data suggest that apelin-13 protects PC12 cells from corticosterone-induced apoptosis through activating PI3K/Akt and ERKs signaling pathways.
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