ArticlePloS one2012
Low-dose alcohol consumption protects against transient focal cerebral ischemia in mice: possible role of PPARγ.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Commonly used anesthetics modify alcohol and (-)-trans-delta9-tetrahydrocannabinol in vivo effects on rat cerebral arterioles.BMC anesthesiology · 2023Article
- Interspecies and regional variability of alcohol action on large cerebral arteries: regulation by KCNMB1 proteins.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Protective Effect of Low-Dose Alcohol Consumption against Post-Ischemic Neuronal Apoptosis: Role of L-PGDS.International journal of molecular sciences · 2021Article
- Chronic Low-Dose Alcohol Consumption Attenuates Post-Ischemic Inflammation via PPARγ in Mice.International journal of molecular sciences · 2021Article
- Chronic Low-Dose Alcohol Consumption Promotes Cerebral Angiogenesis in Mice.Frontiers in cardiovascular medicine · 2021Article
- Influence of low-dose alcohol consumption on post-ischemic inflammation: Role of cystathionine γ-lyase.Alcohol (Fayetteville, N.Y.) · 2019Article
- Dose-Dependent Influences of Ethanol on Ischemic Stroke: Role of Inflammation.Frontiers in cellular neuroscience · 2019Article
- BIRC5 is a novel target of peroxisome proliferator‑activated receptor γ in brain microvascular endothelium cells during cerebral ischemia.Molecular medicine reports · 2017Article
- Effect of Low-Dose Alcohol Consumption on Inflammation Following Transient Focal Cerebral Ischemia in Rats.Scientific reports · 2017Article
- Low-Dose Ethanol Preconditioning Protects Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury By Activating Large Conductance, CaNeuroscience bulletin · 2017Article
- Ethanol-induced changes in poly (ADP ribose) polymerase and neuronal developmental gene expression.Neuropharmacology · 2016Article
- Alcoholic Beverage Consumption and Chronic Diseases.International journal of environmental research and public health · 2016Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe examined the influence of low-dose alcohol consumption on cerebral ischemia/reperfusion (I/R) injury in mice and a potential mechanism underlying the neuroprotective effect of low-dose alcohol consumption. METHODOLOGY/PRINCIPAL
findingsC57BL/6 J mice were fed a liquid diet without or with 1% alcohol for 8 weeks, orally treated with rosiglitazone (20 mg/kg/day), a peroxisome proliferator-activated receptor gamma (PPARγ)-selective agonist, or GW9662 (3 mg/kg/day), a selective PPARγ antagonist, for 2 weeks. The mice were subjected to unilateral middle cerebral artery occlusion (MCAO) for 90 minutes. Brain injury, DNA fragmentation and nuclear PPARγ protein/activity were evaluated at 24 hours of reperfusion. We found that the brain injury and DNA fragmentation were reduced in 1% alcohol-fed mice compared to nonalcohol-fed mice. Rosiglitazone suppressed the brain injury in nonalcohol-fed mice, but didn't alter the brain injury in alcohol-fed mice. In contrast, GW9662 worsened the brain injury in alcohol-fed mice, but didn't alter the brain injury in nonalcohol-fed mice. Nuclear PPARγ protein/activity at peri-infarct and the contralateral corresponding areas of the parietal cortex was greater in alcohol-fed mice compared to nonalcohol-fed mice. Using differentiated catecholaminergic (CATH.a) neurons, we measured dose-related influences of chronic alcohol exposure on nuclear PPARγ protein/activity and the influence of low-dose alcohol exposure on 2-hour oxygen-glucose deprivation (OGD)/24-hour reoxygenation-induced apoptosis. We found that low-dose alcohol exposure increased nuclear PPARγ protein/activity and protected against the OGD/reoxygenation-induced apoptosis. The beneficial effect of low-dose alcohol exposure on OGD/reoxygenation-induced apoptosis was abolished by GW9662. CONCLUSIONS/SIGNIFICANCE: Our findings suggest that chronic consumption of low-dose alcohol protects the brain against I/R injury. The neuroprotective effect of low-dose alcohol consumption may be related to an upregulated PPARγ.
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