ArticleMolecular neurobiology2015
The Neuroprotection of Lysosomotropic Agents in Experimental Subarachnoid Hemorrhage Probably Involving the Apoptosis Pathway Triggering by Cathepsins via Chelating Intralysosomal Iron.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- Underlying Mechanism of Lysosomal Membrane Permeabilization in CNS Injury: A Literature Review.Molecular neurobiology · 2025Review
- A Multi-Target Pharmacological Correction of a LipoyltransferaseAntioxidants (Basel, Switzerland) · 2024Article
- Mechanisms of Ferritinophagy and Ferroptosis in Diseases.Molecular neurobiology · 2024Review
- Article
- Nicotinamide Mononucleotide Adenylyl Transferase 2 Inhibition Aggravates Neurological Damage after Traumatic Brain Injury in a Rat Model.Journal of Korean Neurosurgical Society · 2023Article
- Curcumin activates autophagy and attenuates high glucose-induced apoptosis in HUVECs through the ROS/NF-κB signaling pathway.Experimental and therapeutic medicine · 2022Article
- Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders.Pharmacological reviews · 2022Review
- Roles of Rufy3 in experimental subarachnoid hemorrhage-induced early brain injury via accelerating neuronal axon repair and synaptic plasticity.Molecular brain · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Article
- SOCS1/JAK2/STAT3 axis regulates early brain injury induced by subarachnoid hemorrhage via inflammatory responses.Neural regeneration research · 2021Article
- Eucalyptol ameliorates early brain injury after subarachnoid haemorrhage via antioxidant and anti-inflammatory effects in a rat model.Pharmaceutical biology · 2021Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- Roles of Prokineticin 2 in Subarachnoid Hemorrhage-Induced Early Brain Injury via Regulation of Phenotype Polarization in Astrocytes.Molecular neurobiology · 2020Article
- Cathepsin B in neurodegeneration of Alzheimer's disease, traumatic brain injury, and related brain disorders.Biochimica et biophysica acta. Proteins and proteomics · 2020Review
- Alpha-Lipoic Acid Mediates Clearance of Iron Accumulation by Regulating Iron Metabolism in a Parkinson's Disease Model Induced by 6-OHDA.Frontiers in neuroscience · 2020Article
- Neuroprotection mediated by the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage.Neural regeneration research · 2019Article
- α-Lipoic Acid Reduces Iron-induced Toxicity and Oxidative Stress in a Model of Iron Overload.International journal of molecular sciences · 2019Article
- Pannexin-1 is involved in neuronal apoptosis and degeneration in experimental intracerebral hemorrhage in rats.Molecular medicine reports · 2018Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
α-Lipoic acid-plus (LAP), an amine derivative of α-lipoic acid (LA), could protect cells against oxidant challenges via chelating intralysosomal iron. However, the application of LAP in experimental subarachnoid hemorrhage (SAH) is still not well known. This study was designed to evaluate the potential neuroprotection of LAP on the early brain injury (EBI) and the underlying mechanisms in a rat model of SAH. The SAH models were induced in Sprague-Dawley rats. LA and LAP were oral administration and lasted for 72 h once a day. The brain tissue samples were obtained for assay at 72 h after SAH. In experiment 1, we found that lysosome amounts in neurons decreased significantly in SAH group, and LAP (100 mg/kg) could stabilize lysosomal membrane markedly based on lysosomal-associated membrane protein-1 (LAMP-1) expression in neurons by immunofluorescence. Hence, the LAP dosages of 100 and 150 mg/kg were applied in experiment 2. Firstly, Western blot analysis showed that the protein levels of cathepsin B/D, caspase-3, Bax, ferritin, and heme-oxygenase-1 (HO-1) markedly increased after SAH, which were further confirmed by double immunofluorescence staining and reversed by LA and LAP treatments. In addition, LA and LAP also reduced oxidative stress and iron deposition in brain tissue. Furthermore, LA and LAP significantly ameliorated brain edema, blood-brain barrier injury, cortical apoptosis, and neurological behavior impairment induced by SAH. Finally, it is noteworthy that LAP exerted more significant effects than LA on these parameters as described above. LAP probably exerted neuroprotective effects via targeting lysosomes and chelating intralysosomal iron in EBI post-SAH in rats.
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