ArticleTranslational stroke research2014
Fatty acid methyl esters and Solutol HS 15 confer neuroprotection after focal and global cerebral ischemia.
Article in Translational stroke research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Resveratrol Preconditioning Downregulates PARP1 Protein to Alleviate PARP1-Mediated Cell Death Following Cerebral Ischemia.Translational stroke research · 2024Article
- Activation of Neuropeptide Y2 Receptor Can Inhibit Global Cerebral Ischemia-Induced Brain Injury.Neuromolecular medicine · 2022Article
- Putative Prevention of XML Injection Against Myocardial Ischemia Is Mediated by PKC and PLA2 Proteins.Frontiers in cell and developmental biology · 2022Article
- Palmitic acid methyl ester inhibits cardiac arrest-induced neuroinflammation and mitochondrial dysfunction.Prostaglandins, leukotrienes, and essential fatty acids · 2021Article
- Implication of MicroRNA503 in Brain Endothelial Cell Function and Ischemic Stroke.Translational stroke research · 2020Article
- Stearic acid methyl ester affords neuroprotection and improves functional outcomes after cardiac arrest.Prostaglandins, leukotrienes, and essential fatty acids · 2020Article
- SC411 treatment can enhance survival in a mouse model of sickle cell disease.Prostaglandins, leukotrienes, and essential fatty acids · 2020Article
- Protein Arginine Methyltransferases in Cardiovascular and Neuronal Function.Molecular neurobiology · 2020Review
- Palmitic acid methyl ester is a novel neuroprotective agent against cardiac arrest.Prostaglandins, leukotrienes, and essential fatty acids · 2019Article
- Poster Viewing Sessions PB01-B01 to PB03-V09.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Palmitic Acid Methyl Ester Induces GStem cells international · 2019Article
- Sex-Dependent Differences in Physical Exercise-Mediated Cognitive Recovery Following Middle Cerebral Artery Occlusion in Aged Rats.Frontiers in aging neuroscience · 2019Article
- Whole Body Vibration Therapy after Ischemia Reduces Brain Damage in Reproductively Senescent Female Rats.International journal of molecular sciences · 2018Article
- Cerebral ischemia and neuroregeneration.Neural regeneration research · 2018Review
- Utilizing the Modified T-Maze to Assess Functional Memory Outcomes After Cardiac Arrest.Journal of visualized experiments : JoVE · 2018Article
- Physical Exercise Improves Cognitive Outcomes in 2 Models of Transient Cerebral Ischemia.Stroke · 2017Article
- Effect of cardiac arrest on cognitive impairment and hippocampal plasticity in middle-aged rats.PloS one · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We previously showed that palmitic acid methyl ester (PAME) and stearic acid methyl ester (SAME) are simultaneously released from the sympathetic ganglion and PAME possesses potent vasodilatory properties which may be important in cerebral ischemia. Since PAME is a potent vasodilator simultaneously released with SAME, our hypothesis was that PAME/SAME confers neuroprotection in rat models of focal/global cerebral ischemia. We also examined the neuroprotective properties of Solutol HS15, a clinically approved excipient because it possesses similar fatty acid compositions as PAME/SAME. Asphyxial cardiac arrest (ACA, 6 min) was performed 30 min after PAME/SAME treatment (0.02 mg/kg, IV). Solutol HS15 (2 ml/kg, IP) was injected chronically for 14 days (once daily). Histopathology of hippocampal CA1 neurons was assessed 7 days after ACA. For focal ischemia experiments, PAME, SAME, or Solutol HS15 was administered following reperfusion after 2 h of middle cerebral artery occlusion (MCAO). 2,3,5-Triphenyltetrazolium staining of the brain was performed 24 h after MCAO and the infarct volume was quantified. Following ACA, the number of surviving hippocampal neurons was enhanced by PAME-treated (68%), SAME-treated (69%), and Solutol-treated HS15 (68%) rats as compared to ACA only-treated groups. Infarct volume was decreased by PAME (83%), SAME (68%), and Solutol HS15 (78%) as compared to saline (vehicle) in MCAO-treated animals. PAME, SAME, and Solutol HS15 provide robust neuroprotection in both paradigms of ischemia. This may prove therapeutically beneficial since Solutol HS15 is already administered as a solublizing agent to patients. With proper timing and dosage, administration of Solutol HS15 and PAME/SAME can be an effective therapy against cerebral ischemia.
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