ArticleJournal of neurochemistry2008
Delayed neuronal preconditioning by NS1619 is independent of calcium activated potassium channels.
Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 62 citations in OpenAlex.
- Application of Modulators of CaInternational journal of molecular sciences · 2025Article
- Cerebral Ischemia/Reperfusion Injury and Pharmacologic Preconditioning as a Means to Reduce Stroke-induced Inflammation and Damage.Neurochemical research · 2022Review
- Alternative Targets for Modulators of Mitochondrial Potassium Channels.Molecules (Basel, Switzerland) · 2022Review
- NS1619 Alleviate Brain-Derived Extracellular Vesicle-Induced Brain Injury by Regulating BKca Channel and Nrf2/HO-1/NF-ĸB Pathway.Oxidative medicine and cellular longevity · 2022Article
- BKCardiovascular drugs and therapy · 2021Article
- BK Channels Regulate LPS-induced CCL-2 Release from Human Pulmonary Endothelial Cells.American journal of respiratory cell and molecular biology · 2021Article
- Measuring Respiration in Isolated Murine Brain Mitochondria: Implications for Mechanistic Stroke Studies.Neuromolecular medicine · 2019Article
- Mitochondrial BK Channel Openers CGS7181 and CGS7184 Exhibit Cytotoxic Properties.International journal of molecular sciences · 2018Article
- Preconditioning with the BKAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division.Nature communications · 2017Article
- Role of Mitochondria in Cerebral Vascular Function: Energy Production, Cellular Protection, and Regulation of Vascular Tone.Comprehensive Physiology · 2016Review
- Depolarization of mitochondria in neurons promotes activation of nitric oxide synthase and generation of nitric oxide.American journal of physiology. Heart and circulatory physiology · 2016Article
- The mechanistic target of rapamycin (mTOR) pathway and S6 Kinase mediate diazoxide preconditioning in primary rat cortical neurons.Journal of neurochemistry · 2015Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- The Role of NMDA Receptors in the Development of Brain Resistance through Pre- and Postconditioning.Aging and disease · 2014Review
- Critical role of large-conductance calcium- and voltage-activated potassium channels in leptin-induced neuroprotection of N-methyl-d-aspartate-exposed cortical neurons.Pharmacological research · 2014Article
- Mitochondrial mechanisms in cerebral vascular control: shared signaling pathways with preconditioning.Journal of vascular research · 2014Review
- Mitochondrial respiratory chain and creatine kinase activities following trauma brain injury in brain of mice preconditioned with N-methyl-D-aspartate.Molecular and cellular biochemistry · 2013Article
- Nanoparticle-mediated catalase delivery protects human neurons from oxidative stress.Cell death & disease · 2013Article
- The oxygen free radicals originating from mitochondrial complex I contribute to oxidative brain injury following hypoxia-ischemia in neonatal mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
1,3-Dihydro-1-[2-hydroxy-5-(trifluoromethyl)phenyl]-5-(trifluoromethyl)-2H-benzimidazol-2-one (NS1619), a potent activator of the large conductance Ca2+ activated potassium (BK(Ca)) channel, has been demonstrated to induce preconditioning (PC) in the heart. The aim of our study was to test the delayed PC effect of NS1619 in rat cortical neuronal cultures against oxygen-glucose deprivation, H2O2, or glutamate excitotoxicity. We also investigated its actions on reactive oxygen species (ROS) generation, and on mitochondrial and plasma membrane potentials. Furthermore, we tested the activation of the phosphoinositide 3-kinase (PI3K) signaling pathway, and the effect of NS1619 on caspase-3/7. NS1619 dose-dependently protected the cells against the toxic insults, and the protection was completely blocked by a superoxide dismutase mimetic and a PI3K antagonist, but not by BK(Ca) channel inhibitors. Application of NS1619 increased ROS generation, depolarized isolated mitochondria, hyperpolarized the neuronal cell membrane, and activated the PI3K signaling cascade. However, only the effect on the cell membrane potential was antagonized by BK(Ca) channel blockers. NS1619 inhibited the activation of capase-3/7. In summary, NS1619 is a potent inducer of delayed neuronal PC. However, the neuroprotective effect seems to be independent of cell membrane and mitochondrial BK(Ca) channels. Rather it is the consequence of ROS generation, activation of the PI3K pathway, and inhibition of caspase activation.
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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.