ArticleOxidative medicine and cellular longevity2022
ACEA Attenuates Oxidative Stress by Promoting Mitophagy via CB1R/Nrf1/PINK1 Pathway after Subarachnoid Hemorrhage in Rats.
Article in Oxidative medicine and cellular longevity, 2022. 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.
- Mitophagy alleviates neuronal damage after subarachnoid hemorrhage: Role of autophagy-targeting chimera 4.Neural regeneration research · 2026Article
- Photobiomodulation repairs the blood-spinal cord barrier in a mouse model of spinal cord injury.Neural regeneration research · 2026Article
- Effect of sevoflurane versus propofol on immune inflammation in patients undergoing endovascular coiling of cerebral aneurysm.BMC anesthesiology · 2026Observational
- Hypoxia preconditioned MSC exosomes attenuate high-altitude cerebral edema via the miR-125a-5p/RTEF-1 axis to protect vascular endothelial cells.Bioactive materials · 2025Article
- Retinoic acid-inducible gene-I aggravates neuroinflammation in early brain injury after subarachnoid hemorrhage through mediating brain microvascular endothelial cell pyroptosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Itaconate promotes mitophagy to inhibit neuronal ferroptosis after subarachnoid hemorrhage.Apoptosis : an international journal on programmed cell death · 2025Article
- Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- Longitudinal change and prognostic significance of serum PINK1 levels, and mediation role of delayed cerebral ischemia in human aneurysmal subarachnoid hemorrhage: an observational analytical study.Frontiers in neurology · 2025Article
- Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage.Neural regeneration research · 2024Review
- Berberine alleviates ischemia reperfusion injury induced AKI by regulation of intestinal microbiota and reducing intestinal inflammation.BMC complementary medicine and therapies · 2024Article
- Connection between oxidative stress and subcellular organelle in subarachnoid hemorrhage: Novel mechanisms and therapeutic implications.CNS neuroscience & therapeutics · 2023Review
- Neuroprotection and Beyond: The Central Role of CB1 and CB2 Receptors in Stroke Recovery.International journal of molecular sciences · 2023Review
- RU.521 mitigates subarachnoid hemorrhage-induced brain injury via regulating microglial polarization and neuroinflammation mediated by the cGAS/STING/NF-κB pathway.Cell communication and signaling : CCS · 2023Article
- The Cannabinoid Ligand Arachidonyl-2'-Chloroethylamide (ACEA) Ameliorates Depressive and Overactive Bladder Symptoms in a Corticosterone-Induced Female Wistar Rat Model.International journal of molecular sciences · 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
- Caveolin-1 accelerates hypoxia-induced endothelial dysfunction in high-altitude cerebral edema.Cell communication and signaling : CCS · 2022Article
- Molecular mechanisms of neuronal death in brain injury after subarachnoid hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Cycloastragenol Confers Cerebral Protection after Subarachnoid Hemorrhage by Suppressing Oxidative Insults and Neuroinflammation via the SIRT1 Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
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7 authors.
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Abstract
methodEndovascular perforation was performed to establish a SAH model of rats. ACEA was administered intraperitoneally 1 h after SAH. The CB1R antagonist AM251 was injected intraperitoneally 1 h before SAH induction. Adenoassociated virus- (AAV-) Nrf1 shRNA was infused into the lateral ventricle 3 weeks before SAH induction. Neurological tests, immunofluorescence, DHE, TUNEL, Nissl staining, transmission electron microscopy (TEM), and Western blot were performed.
resultsThe expression of CB1R, Nrf1, PINK1, Parkin, and LC3II increased and peaked at 24 h after SAH. ACEA treatment exhibited the antioxidative stress and antiapoptosis effects after SAH. In addition, ACEA treatment increased the expression of Nrf1, PINK1, Parkin, LC3II, and Bcl-xl but repressed the expression of Romo-1, Bax, and cleaved caspase-3. Moreover, the TEM results demonstrated that ACEA promoted the formation of mitophagosome and maintained the normal mitochondrial morphology of neurons. The protective effect of ACEA was reversed by AM251 and Nrf1 shRNA, respectively.
conclusionsThis study demonstrated that ACEA alleviated oxidative stress and neurological dysfunction by promoting mitophagy after SAH, at least in part via the CB1R/Nrf1/PINK1 signaling pathway.
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