ArticleNeuropharmacology2018
Exendin-4 attenuates neuronal death via GLP-1R/PI3K/Akt pathway in early brain injury after subarachnoid hemorrhage in rats.
Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 97 citations in OpenAlex.
- The Pleiotropic Therapeutic Perspectives of GLP-1 and GIP Receptor Agonists in Spinal Cord Injury: A Narrative Review.Molecular neurobiology · 2026Review
- Converging neurotrophic-immune signaling in autism spectrum disorder: integrative roles of klotho, GDNF/GFRA-1, IGF-1 and GLP-1 pathways.Metabolic brain disease · 2026Review
- GLP-1 and GIP: Magic bullet for musculoskeletal diseases?Journal of advanced research · 2026Review
- NDRG4 overexpression is associated with reduced apoptosis after intracerebral hemorrhage via the PI3K/Akt/GSK3β signaling pathway.Scientific reports · 2026Article
- Effects of Glucagon-Like Peptide-1 Receptor Agonist on Bone Metabolism and the Expression of Insulin Receptor Substrate 1 in an Osteoporotic Rat Model.International journal of endocrinology · 2026Article
- Incretin Mimetics as Potential Therapeutics for Concussion and Traumatic Brain Injury: A Narrative Review.International journal of molecular sciences · 2025Review
- The potential role of GLP-1 receptor agonists in the management of psoriatic disease: a scoping review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- GLP-1 Receptor Agonists and Clinical Outcomes after Endovascular Treatment of Unruptured Aneurysms in Type 2 Diabetes.Stroke (Hoboken, N.J.) · 2025Article
- The Potential Protective Effects of Intermittent Fasting Against Radiation-Induced Brain Damage in a Rat Model: Suggested Involvement of IRS-1/PI3 K/AKT and BDNF/TrkB Signaling Pathways.Molecular neurobiology · 2025Article
- Comparative outcomes of systemic diseases in people with type 2 diabetes, or obesity alone treated with and without GLP-1 receptor agonists: a retrospective cohort study from the Global Collaborative Network : Author list.Journal of endocrinological investigation · 2025Article
- Exosomal miR-450b-5p Secreted from Exendin-4-Stimulated Endothelial Cells Protects Retinal Ganglion Cells Against Ischemia Reperfusion Injury.International journal of nanomedicine · 2025Article
- GLP-1 Receptor Agonists: Beyond Diabetes-What the Neurosurgeon Needs to Know.Neurosurgery practice · 2024Review
- MFGE8 promotes adult hippocampal neurogenesis in rats following experimental subarachnoid hemorrhage via modifying the integrin β3/Akt signaling pathway.Cell death discovery · 2024Article
- Diabetes drugs activate neuroprotective pathways in models of neonatal hypoxic-ischemic encephalopathy.EMBO molecular medicine · 2024Article
- Exendin-4 Prevents Memory Loss and Neuronal Death in Rats with Sporadic Alzheimer-Like Disease.Molecular neurobiology · 2024Article
- Alpha-Asarone Ameliorates Neurological Dysfunction of Subarachnoid Hemorrhagic Rats in Both Acute and Recovery Phases via Regulating the CaMKII-Dependent Pathways.Translational stroke research · 2024Article
- Inhibiting PI3K/Akt-Signaling Pathway Improves Neurobehavior Changes in Anti-NMDAR Encephalitis Mice by Ameliorating Blood-Brain Barrier Disruption and Neuronal Damage.Cellular and molecular neurobiology · 2023Article
- ASK1 inhibitor NQDI‑1 decreases oxidative stress and neuroapoptosis via the ASK1/p38 and JNK signaling pathway in early brain injury after subarachnoid hemorrhage in rats.Molecular medicine reports · 2023Article
- Glucagon-like peptide-1 (GLP-1) receptor agonists and neuroinflammation: Implications for neurodegenerative disease treatment.Pharmacological research · 2022Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Neuronal apoptosis is considered to be a crucial therapeutic target against early brain injury (EBI) after subarachnoid hemorrhage (SAH). Emerging evidence indicates that Exendin-4 (Ex-4), a glucagon-like peptide 1 receptor (GLP-1R) agonist, plays a neuroprotective role in cerebrovascular disease. This study was conducted in order to verify the neuroprotective role of EX-4 in EBI after SAH in rats. The endovascular perforation model of SAH was performed in Sprague-Dawley rats (n = 153). Ex-4 was intraperitoneally injected 1 h after SAH induction in the rats (SAH + Ex-4). To elucidate the underlying molecular mechanism, small interfering ribonucleic acid (siRNA) for GLP-1R and a specific inhibitor of PI3K, LY294002, were injected intracerebroventricularly into SAH + Ex-4 rats before induction of SAH (n = 6 per group). SAH grading evaluation, immunohistochemistry, Western blots, neurobehavioral assessment, and Fluoro-Jade C (FJC) staining experiments were performed. Expression of GLP-1R was significantly increased and mainly expressed in neurons at 24 h after SAH induction. Administration of Ex-4 significantly improved both short- and long-term neurobehavior in SAH + Ex-4 group compared to SAH + Vehicle group after SAH. Ex-4 treatment significantly increased the expression of GLP-1R, PI3K, p-Akt, Bcl-xl, and Bcl-2, while at the same time was found to decrease expression of Bax in the brain. Effects of Ex-4 were reversed by the intervention of GLP-1R siRNA and LY294002 in SAH + Ex-4+GLP-1R siRNA and SAH + Ex-4+LY294002 groups, respectively. In conclusion, the neuroprotective effect of Ex-4 in EBI after SAH was mediated by attenuation of neuronal apoptosis via GLP-1R/PI3K/Akt signaling pathway, therefore EX-4 should be further investigated as a potential therapeutic agent in stroke patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.