ArticleFrontiers in pharmacology2014
Soluble epoxide hydrolase gene deletion improves blood flow and reduces infarct size after cerebral ischemia in reproductively senescent female mice.
Article in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Endothelial expression of human soluble epoxide hydrolase worsens acute microvascular and tissue injury after stroke in female mice with early-stage diabetes mellitus.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Alterations in mitochondria and cellular senescence in aged sEH null female kidneys.GeroScience · 2026Article
- Article
- Epoxide Hydrolase Inhibitors for the Treatment of Alzheimer's Disease and Other Neurological Disorders: A Comprehensive Review.Biomedicines · 2025Review
- Effects of molecular interactions between the exposome and oxylipin metabolism on healthspan.Frontiers in physiology · 2025Review
- Article
- Soluble Epoxide Hydrolase Inhibitor Ameliorates Olfactory Dysfunction, Modulates Microglia Polarization, and Attenuates Neuroinflammation after Ischemic Brain Injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Soluble epoxide hydrolase inhibitor blockage microglial cell activation in subnucleus caudalis in a persistent model of arthritis.International immunopharmacology · 2023Article
- Soluble Epoxide Hydrolase Contributes to Cell Senescence and ER Stress in Aging Mice Colon.International journal of molecular sciences · 2023Article
- Identifying genetic variants for amyloid β in subcortical vascular cognitive impairment.Frontiers in aging neuroscience · 2023Article
- Research progress on the protective mechanism of a novel soluble epoxide hydrolase inhibitor TPPU on ischemic stroke.Frontiers in neurology · 2023Review
- Soluble Epoxide Hydrolase Is Associated with Postprandial Anxiety Decrease in Healthy Adult Women.International journal of molecular sciences · 2022Article
- A Review of Oxylipins in Alzheimer's Disease and Related Dementias (ADRD): Potential Therapeutic Targets for the Modulation of Vascular Tone and Inflammation.Metabolites · 2022Review
- Impact of diabetes and ischemic stroke on the cerebrovasculature: A female perspective.Neurobiology of disease · 2022Review
- Lipids as Regulators of Cellular Senescence.Frontiers in physiology · 2022Review
- Soluble Epoxide Hydrolase in Aged Female Mice and Human Explanted Hearts Following Ischemic Injury.International journal of molecular sciences · 2021Article
- sEH Inhibitor Tppu Ameliorates Cecal Ligation and Puncture-Induced Sepsis by Regulating Macrophage Functions.Shock (Augusta, Ga.) · 2020Article
- 1-Trifluoromethoxyphenyl-3-(1-Propionylpiperidin-4-yl) Urea Protects the Blood-Brain Barrier Against Ischemic Injury by Upregulating Tight Junction Protein Expression, Mitigating Apoptosis and InflammationFrontiers in pharmacology · 2020Article
- Protective Effects of the Soluble Epoxide Hydrolase Inhibitor 1-Trifluoromethoxyphenyl-3-(1-Propionylpiperidin-4-yl) Urea in a Rat Model of Permanent Middle Cerebral Artery Occlusion.Frontiers in pharmacology · 2020Article
- Genistein Attenuates Acute Cerebral Ischemic Damage by Inhibiting the NLRP3 Inflammasome in Reproductively Senescent Mice.Frontiers in aging neuroscience · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Soluble epoxide hydrolase (sEH), a key enzyme in the metabolism of vasodilatory epoxyeicosatrienoic acids (EETs), is sexually dimorphic, suppressed by estrogen, and contributes to underlying sex differences in cerebral blood flow and injury after cerebral ischemia. We tested the hypothesis that sEH inhibition or gene deletion in reproductively senescent (RS) female mice would increase cerebral perfusion and decrease infarct size following stroke. RS (15-18 month old) and young (3-4 month old) female sEH knockout (sEHKO) mice and wild type (WT) mice were subjected to 45 min middle cerebral artery occlusion (MCAO) with laser Doppler perfusion monitoring. WT mice were treated with vehicle or a sEH inhibitor t-AUCB at the time of reperfusion and every 24 h thereafter for 3 days. Differences in regional cerebral blood flow were measured in vivo using optical microangiography (OMAG). Infarct size was measured 3 days after reperfusion. Infarct size and cerebral perfusion 24 h after MCAO were not altered by age. Both sEH gene deletion and sEH inhibition increased cortical perfusion 24 h after MCAO. Neither sEH gene deletion nor sEH inhibition reduced infarct size in young mice. However, sEH gene deletion, but not sEH inhibition of the hydrolase domain of the enzyme, decreased infarct size in RS mice. Results of these studies show that sEH gene deletion and sEH inhibition enhance cortical perfusion following MCAO and sEH gene deletion reduces damage after ischemia in RS female mice; however this neuroprotection in absent is young mice.
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