ArticleInternational journal of molecular sciences2018
Nicotine Alters Estrogen Receptor-Beta-Regulated Inflammasome Activity and Exacerbates Ischemic Brain Damage in Female Rats.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Nicotine-Mediated Alterations in Exosome Content: Implications for Stroke and Neurological Dysfunction.Biomolecules · 2026Review
- Targeting the NLRP3 inflammasome with natural products for ischemia-reperfusion injury across organs: mechanisms, structure-activity relationships, and delivery innovations.Inflammopharmacology · 2025Review
- Nicotine is an Immunosuppressant: Implications for Women's Health and Disease.Journal of neuroimmunology · 2024Review
- E-cigarette vapor extract alters human eosinophil gene expression in an effect mediated by propylene glycol, glycerin, and nicotine.Journal of leukocyte biology · 2024Article
- The Role of Licorice Chalcones as Molecular Genes and Signaling Pathways Modulator-A Review of Experimental Implications for Nicotine-Induced Non-Small Cell Lung Cancer Treatment.Current issues in molecular biology · 2024Review
- Linking alterations in estrogen receptor expression to memory deficits and depressive behavior in an ovariectomy mouse model.Scientific reports · 2024Article
- Role of estrogen in sex differences in memory, emotion and neuropsychiatric disorders.Molecular biology reports · 2024Review
- Electronic Cigarette Vape Exposure Exacerbates Post-Ischemic Outcomes in Female but Not in Male Rats.Stroke · 2024Article
- Article
- NLRP3 Inflammasome Pharmacological Inhibitors inJournal of inflammation research · 2022Review
- Nicotine Exposure Along with Oral Contraceptive Treatment in Female Rats Exacerbates Post-cerebral Ischemic Hypoperfusion Potentially via Altered Histamine Metabolism.Translational stroke research · 2021Article
- Simultaneous nicotine and oral contraceptive exposure alters brain energy metabolism and exacerbates ischemic stroke injury in female rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Improving translational research in sex-specific effects of comorbidities and risk factors in ischaemic heart disease and cardioprotection: position paper and recommendations of the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2021Review
- Nuclear Receptors in the Control of the NLRP3 Inflammasome Pathway.Frontiers in endocrinology · 2021Review
- New Mechanistic Insights, Novel Treatment Paradigms, and Clinical Progress in Cerebrovascular Diseases.Frontiers in aging neuroscience · 2021Article
- The peri-menopause in a woman's life: a systemic inflammatory phase that enables later neurodegenerative disease.Journal of neuroinflammation · 2020Review
- Estrogen preconditioning: A promising strategy to reduce inflammation in the ischemic brain.Conditioning medicine · 2019Article
- Molecular Pathways of Estrogen Receptor Action.International journal of molecular sciences · 2018Article
- Mitochondrial Dysfunction in Stroke: Implications of Stem Cell Therapy.Translational stroke research · 2018Review
- Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smoking is a preventable risk factor for stroke and smoking-derived nicotine exacerbates post-ischemic damage via inhibition of estrogen receptor beta (ER-β) signaling in the brain of female rats. ER-β regulates inflammasome activation in the brain. Therefore, we hypothesized that chronic nicotine exposure activates the inflammasome in the brain, thus exacerbating ischemic brain damage in female rats. To test this hypothesis, adult female Sprague-Dawley rats (6⁻7 months old) were exposed to nicotine (4.5 mg/kg/day) or saline for 16 days. Subsequently, brain tissue was collected for immunoblot analysis. In addition, another set of rats underwent transient middle cerebral artery occlusion (tMCAO; 90 min) with or without nicotine exposure. One month after tMCAO, histopathological analysis revealed a significant increase in infarct volume in the nicotine-treated group (64.24 ± 7.3 mm³; mean ± SEM;
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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.