ArticleExperimental and therapeutic medicine2014
Progesterone alleviates hypoxic-ischemic brain injury via the Akt/GSK-3β signaling pathway.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Ganaxolone as a promising therapeutic agent for Alzheimer's disease: signaling pathways and mechanistic insights-a narrative review.Inflammopharmacology · 2026Review
- Akt-activated GSK3β inhibitory peptide effectively blocks tau hyperphosphorylation.Archives of pharmacal research · 2024Article
- Therapeutic Interventions in Rat Models of Preterm Hypoxic Ischemic Injury: Effects of Hypothermia, Caffeine, and the Influence of Sex.Life (Basel, Switzerland) · 2022Review
- Article
- Long-Lasting Actions of Progesterone Protect the Neonatal Brain Following Hypoxia-Ischemia.Cellular and molecular neurobiology · 2020Article
- O-GlcNAc impairs endothelial function in uterine arteries from virgin but not pregnant rats: The role of GSK3β.European journal of pharmacology · 2020Article
- Repurposing antimycotic ciclopirox olamine as a promising anti-ischemic stroke agent.Acta pharmaceutica Sinica. B · 2020Article
- Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway.Brain sciences · 2019Article
- A11, a novel diaryl acylhydrazone derivative, exerts neuroprotection against ischemic injury in vitro and in vivo.Acta pharmacologica Sinica · 2019Article
- Mangiferin Potentiates Neuroprotection by Isoflurane in Neonatal Hypoxic Brain Injury by Reducing Oxidative Stress and Activation of Phosphatidylinositol-3-Kinase/Akt/Mammalian Target of Rapamycin (PI3K/Akt/mTOR) Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Effects of progesterone on the neonatal brain following hypoxia-ischemia.Metabolic brain disease · 2018Article
- Sex Differences in Autophagy Contribute to Female Vulnerability in Alzheimer's Disease.Frontiers in neuroscience · 2018Review
- Cell Death in the Developing Brain after Hypoxia-Ischemia.Frontiers in cellular neuroscience · 2017Review
- Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.Neuropharmacology · 2016Review
- Use of estetrol with other steroids for attenuation of neonatal hypoxic-ischemic brain injury: to combine or not to combine?Oncotarget · 2016Article
- Protective effects of monosialotetrahexosylganglioside sodium on HExperimental and therapeutic medicine · 2015Article
- Perspective of synaptic protection after post-infarction treatment with statins.Journal of translational medicine · 2015Review
- Pretreatment with Resveratrol Prevents Neuronal Injury and Cognitive Deficits Induced by Perinatal Hypoxia-Ischemia in Rats.PloS one · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This aim of this study was to investigate whether progesterone (PROG) alleviates the neuronal apoptosis in neonatal rats with hypoxic-ischemic (HI) brain damage through the phosphatidylinositol 3-kinase (PI3K)/Akt/glycogen synthase kinase-3β (GSK-3β) signaling pathway. A total of 96 newborn Wistar rats aged 7 days were randomly divided into four groups: sham surgery, HI, drug prevention (PROG) and Akt inhibitor groups. HI animal models were established by a conventional method. All animals were sacrificed 24 h after hypoxia. Immunohistochemistry was used to detect the distribution and expression of phosphorylated Akt (p-Akt) and the GSK-3β proteins in the brain, and western blot analysis was used to determine the p-Akt and GSK-3β protein contents. An enzyme-linked immunosorbent assay was also used to determine the GSK-3β content of the brain tissue, and flow cytometry was used to evaluate the apoptosis rate of neural cells. The expression of p-Akt protein was reduced in the brain tissues of the HI group, whereas GSK-3β expression was increased. In addition, the GSK-3β content of the brain and the neuronal apoptosis rate were significantly increased. PROG pre-treatment increased p-Akt expression, decreased GSK-3β expression and GSK-3β content, and also reduced neuronal apoptosis. Following administration of the Akt inhibitor wortmannin, p-Akt expression decreased, GSK-3β expression increased, and the GSK-3β content and neuronal apoptosis rate significantly increased (P<0.05). In conclusion, PROG activates the PI3K/Akt/GSK-3β pathway to promote Akt activation, enhance p-Akt expression and inhibit GSK-3β expression, thereby inhibiting neuronal apoptosis, alleviating HI brain injury and inducing a cerebroprotective effect.
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