ArticleRedox biology2019
AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 189 citations in OpenAlex.
- Mas receptor activation regulates the functional phenotype of myocardial macrophages through the Akt/Nrf2 signaling pathway to alleviate sepsis-induced cardiomyopathy.Journal of translational medicine · 2026Article
- Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026Review
- SIRT2 Inhibition promotes microglia LC3-associated phagocytosis via NRF2/CD36 after the experimental subarachnoid hemorrhage.Journal of neuroinflammation · 2025Article
- Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.Inflammopharmacology · 2025Article
- miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation.Scientific reports · 2025Article
- Inhibition of histone deacetylase 6 activity mitigates neurological impairment and post-hemorrhagic hydrocephalus after intraventricular hemorrhage by modulating pyroptosis and autophagy pathways.Fluids and barriers of the CNS · 2025Article
- Research progress of early brain Injury in subarachnoid hemorrhage from 2004 to 2024: a bibliometric analysis.Neurosurgical review · 2025Review
- Activation of central Angiotensin-(1-7)/Mas receptor alleviates synaptic damage in diabetes-associated cognitive impairment via modulating AKT/FOXO1/PACAP axis.International journal of biological sciences · 2025Article
- Nitric Oxide Metabolite Improves Cognitive Impairment by Reducing the Loss of Parvalbumin Inhibitory Interneurons in a Novel Mouse Model of Vascular Dementia.Current neuropharmacology · 2025Article
- Identification of mRNA biomarkers in extremely early hypertensive intracerebral hemorrhage (HICH).Proteome science · 2024Article
- Oxytocin Protects Against Corticosterone-Induced DA Dysfunction: An Involvement of the PKA/CREB Pathway.Neurochemical research · 2024Article
- Review
- Betulin ameliorates neuronal apoptosis and oxidative injury via DJ-1/Akt/Nrf2 signaling pathway after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition.Acta biochimica et biophysica Sinica · 2024Article
- Mas receptor activation facilitates innate hematoma resolution and neurological recovery after hemorrhagic stroke in mice.Journal of neuroinflammation · 2024Article
- Rasd1 is involved in white matter injury through neuron-oligodendrocyte communication after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Intranasal administration of recombinant prosaposin attenuates neuronal apoptosis through GPR37/PI3K/Akt/ASK1 pathway in MCAO rats.Experimental neurology · 2024Article
- Edaravone dexborneol attenuates oxidative stress in experimental subarachnoid hemorrhage via Keap1/Nrf2 signaling pathway.Frontiers in pharmacology · 2024Article
- Perampanel attenuates oxidative stress and pyroptosis following subarachnoid hemorrhage via the SIRT3/FOXO3α pathway.Scientific reports · 2023Article
- Astaxanthin attenuates cognitive deficits in Alzheimer's disease models by reducing oxidative stress via the SIRT1/PGC-1α signaling pathway.Cell & bioscience · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Oxidative stress and neuronal apoptosis have been demonstrated to be key features in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Previous studies have indicated that Mas receptor activation initiates an anti-oxidative and anti-apoptotic role in the brain. However, whether Mas activation can attenuate oxidative stress and neuronal apoptosis after SAH remains unknown. To investigate the beneficial effect of Mas on oxidative stress injury and neuronal apoptosis induced by SAH, a total of 196 rats were subjected to an endovascular perforation model of SAH. AVE 0991 (AVE), a selective agonist of Mas, was administered intranasally 1 h after SAH induction. A779, a selective inhibitor of Mas, and small interfering ribonucleic acid (siRNA) for UCP-2 were administered by intracerebroventricular (i.c.v) injection at 1 h and 48 h before SAH induction respectively. Neurological tests, immunofluorescence, TUNEL, Fluoro-Jade C, DHE staining, and Western blot experiments were performed. We found that Mas activation with AVE significantly improved neurobehavioral scores and reduced oxidative stress and neuronal apoptosis in SAH+AVE group compared with SAH+vehicle group. Moreover, AVE treatment significantly promoted phosphorylation of CREB and the expression UCP-2, as well as upregulated expression of Bcl-2 and downregulation of Romo-1 and Bax. The protective effects of AVE were reversed by i.c.v injection of A779 and UCP-2 siRNA in SAH+AVE+A779 and SAH+AVE+UCP-2 siRNA groups, respectively. In conclusion, our data provides evidence that Mas activation with AVE reduces oxidative stress injury and neuronal apoptosis through Mas/PKA/p-CREB/UCP-2 pathway after SAH. Furthermore, our study indicates that Mas may be a novel therapeutic treatment target in early brain injury of SAH.
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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.