ArticleMolecular brain2009
Cocaine induces cell death and activates the transcription nuclear factor kappa-B in PC12 cells.
Article in Molecular brain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 68 citations in OpenAlex.
- The landscape of cocaine cytotoxicity and the role of sigma-1 receptor modulation and adulterant synergism.Archives of toxicology · 2026Review
- Dimethyltryptamine and harmine, components of ayahuasca, prevented cocaine-induced apoptosis in SH-SY5Y human neuroblastoma cells.Archives of toxicology · 2026Article
- LY-2183240 enhances reward-seeking behavior with inducing neuronal excitation and early apoptosis in mouse.iScience · 2024Article
- Nuclear factor kappa B signaling within the rat nucleus accumbens core sex-dependently regulates cue-induced cocaine seeking and matrix metalloproteinase-9 expression.Brain, behavior, and immunity · 2022Article
- Anhydroecgonine methyl ester, a cocaine pyrolysis product, contributes to cocaine-induced rat primary hippocampal neuronal death in a synergistic and time-dependent manner.Archives of toxicology · 2021Article
- Anhydroecgonine methyl ester (AEME), a cocaine pyrolysis product, impairs glutathione-related enzymes response and increases lipid peroxidation in the hippocampal cell culture.Toxicology reports · 2019Article
- Identification of biochemical and cytotoxic markers in cocaine treated PC12 cells.Scientific reports · 2018Article
- Monoaminergic toxicity induced by cathinone phthalimide: An in vitro study.Neuroscience letters · 2017Article
- Global cocaine intoxication research trends during 1975-2015: a bibliometric analysis of Web of Science publications.Substance abuse treatment, prevention, and policy · 2017Article
- Cocaine Enhances HIV-1 Transcription in Macrophages by Inducing p38 MAPK Phosphorylation.Frontiers in microbiology · 2016Article
- Suppression of MAPK attenuates neuronal cell death induced by activated glia-conditioned medium in alpha-synuclein overexpressing SH-SY5Y cells.Journal of neuroinflammation · 2015Article
- A Comprehensive View of the Neurotoxicity Mechanisms of Cocaine and Ethanol.Neurotoxicity research · 2015Review
- Cocaine induces nuclear export and degradation of neuronal retinoid X receptor-γ via a TNF-α/JNK- mediated mechanism.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015Article
- Cocaine Causes Apoptotic Death in Rat Mesencephalon and Striatum Primary Cultures.BioMed research international · 2015Article
- Intermittent fasting attenuates lipopolysaccharide-induced neuroinflammation and memory impairment.Journal of neuroinflammation · 2014Article
- Cocaine disrupts histamine H3 receptor modulation of dopamine D1 receptor signaling: σ1-D1-H3 receptor complexes as key targets for reducing cocaine's effects.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Enhanced expression of WD repeat-containing protein 35 via nuclear factor-kappa B activation in bupivacaine-treated Neuro2a cells.PloS one · 2014Article
- Serine racemase: a key player in apoptosis and necrosis.Frontiers in synaptic neuroscience · 2014Review
- Influence of the dopaminergic system, CREB, and transcription factor-κB on cocaine neurotoxicity.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2013Article
- Nitric oxide and histone deacetylases modulate cocaine-induced mu-opioid receptor levels in PC12 cells.BMC pharmacology & toxicology · 2012Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cocaine is a worldwide used drug and its abuse is associated with physical, psychiatric and social problems. The mechanism by which cocaine causes neurological damage is very complex and involves several neurotransmitter systems. For example, cocaine increases extracellular levels of dopamine and free radicals, and modulates several transcription factors. NF-kappaB is a transcription factor that regulates gene expression involved in cellular death. Our aim was to investigate the toxicity and modulation of NF-kappaB activity by cocaine in PC 12 cells. Treatment with cocaine (1 mM) for 24 hours induced DNA fragmentation, cellular membrane rupture and reduction of mitochondrial activity. A decrease in Bcl-2 protein and mRNA levels, and an increase in caspase 3 activity and cleavage were also observed. In addition, cocaine (after 6 hours treatment) activated the p50/p65 subunit of NF-kappaB complex and the pretreatment of the cells with SCH 23390, a D1 receptor antagonist, attenuated the NF-kappaB activation. Inhibition of NF-kappaB activity by using PDTC and Sodium Salicilate increased cell death caused by cocaine. These results suggest that cocaine induces cell death (apoptosis and necrosis) and activates NF-kappaB in PC12 cells. This activation occurs, at least partially, due to activation of D1 receptors and seems to have an anti-apoptotic effect on these cells.
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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.