ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022
An apoptosis inhibitor suppresses microglial and astrocytic activation after cardiac ischemia/reperfusion injury.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Metabolism-Mediated Regulation of Brain-Heart Interactions.International journal of molecular sciences · 2026Review
- Electroacupuncture Pretreatment Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting Engulfment by Microglia in the Lateral Hypothalamus.CNS neuroscience & therapeutics · 2025Article
- Aerobic Exercise Activates Fibroblast Growth Factor 21 and Alleviates Cardiac Ischemia/Reperfusion-induced Neuronal Oxidative Stress and Ferroptosis in Paraventricular Nucleus.Molecular neurobiology · 2025Article
- Hyperoside ameliorates lupus nephritis by suppressing AKT1-mediated PANoptosis in podocytes: integrating network pharmacology and experimental validation.Frontiers in pharmacology · 2025Article
- Communication Regarding the Myocardial Ischemia/Reperfusion and Cognitive Impairment: A Narrative Literature Review.Journal of Alzheimer's disease : JAD · 2024Review
- Global Research Trends on Exosome in Cardiovascular Diseases: A Bibliometric-Based Visual Analysis.Vascular health and risk management · 2024Review
- Electroacupuncture attenuates myocardial ischemia-reperfusion injury by inhibiting microglial engulfment of dendritic spines.iScience · 2023Article
- Spinal cord astrocytes regulate myocardial ischemia-reperfusion injury.Basic research in cardiology · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveMicroglial hyperactivation and apoptosis were observed following myocardial infarction and ischemia reperfusion (I/R) injury. This study aimed to test the hypothesis that the apoptosis inhibitor, Z-VAD, attenuates microglial and astrocytic hyperactivation and brain inflammation in rats with cardiac I/R injury. MATERIALS AND
methodsRats were subjected to either sham or cardiac I/R operation (30 min-ischemia followed by 120-min reperfusion), rats in the cardiac I/R group were given either normal saline solution or Z-VAD at 3.3 mg/kg via intravenous injection 15 min prior to cardiac ischemia. Left ventricular ejection fraction (% LVEF) was determined during the cardiac I/R protocol. The brain tissues were removed and used to determine brain apoptosis, brain inflammation, microglial and astrocyte morphology.
resultsCardiac dysfunction was observed in rats with cardiac I/R injury as indicated by decreased %LVEF. In the brain, we found brain apoptosis, brain inflammation, microglia hyperactivation, and reactive astrogliosis occurred following cardiac I/R injury. Pretreatment with Z-VAD effectively increased %LVEF, reduced brain apoptosis, attenuated brain inflammation by decreasing IL-1β mRNA levels, suppressed microglial and astrocytic hyperactivation and proliferation after cardiac I/R injury.
conclusionZ-VAD exerts neuroprotective effects against cardiac I/R injury not only targeting apoptosis but also microglial and astrocyte activation.
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