ArticleActa pharmacologica Sinica2011
Combined prostaglandin E1 and lithium exert potent neuroprotection in a rat model of cerebral ischemia.
Article in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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14 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Method parameters' impact on mortality and variability in rat stroke experiments: a meta-analysis.BMC neuroscience · 2013Pooled it
- Cognitive Impairment Associated with Chemotherapy: Neuroimmunological Interactions, Gut-Brain Axis, and Therapeutic Approaches.Brain sciences · 2026Review
- Combination drug therapy prevents CIAKI by suppressing ER stress-induced apoptosis.Scientific reports · 2024Article
- Chaperones vs. oxidative stress in the pathobiology of ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2023Review
- PGE1 triggers Nrf2/HO-1 signal pathway to resist hemin-induced toxicity in mouse cortical neurons.Annals of translational medicine · 2021Article
- Prostaglandin E1 Improves Cerebral Microcirculation Through Activation of Endothelial NOS and GRPCH1.Journal of molecular neuroscience : MN · 2020Article
- Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics.Frontiers in neuroscience · 2019Article
- Lipo‑prostaglandin E1 modifies cognitive impairment in rats with vascular cognitive impairment by promoting angiogenesis via the VEGF/VEGFR pathway.Molecular medicine reports · 2017Article
- TIGAR contributes to ischemic tolerance induced by cerebral preconditioning through scavenging of reactive oxygen species and inhibition of apoptosis.Scientific reports · 2016Article
- Protease Omi cleaving Hax-1 protein contributes to OGD/R-induced mitochondrial damage in neuroblastoma N2a cells and cerebral injury in MCAO mice.Acta pharmacologica Sinica · 2015Article
- Treatment of acute cerebral ischemia using animal models: a meta-analysis.Translational neuroscience · 2015Review
- Effects of Acute Lithium Treatment on Brain Levels of Inflammatory Mediators in Poststroke Rats.BioMed research international · 2015Article
- Lithium protects against glucocorticoid induced neural progenitor cell apoptosis in the developing cerebellum.Brain research · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo examine the effects of a mixed formulation composed of prostaglandin E1 and lithium (PGE1+Li mixture) on brain damage after cerebral ischemia. The effects of the mixture on protein expression of heat shock proteins (HSPs), p53, and Bcl-2 were also determined.
methodsBrain ischemia was induced with a permanent middle cerebral artery occlusion (pMCAO) in rats. Rats were treated with a single intravenous administration of PGE1, lithium or a PGE1+Li mixture immediately after the ischemic insult. The infarct volume and motor behavior deficits were analyzed 24 h after the ischemic insult. The protein levels of HSP70, glucose-regulated protein 78 (GRP78), HSP60, Bcl-2, and p53 in the striatum of the ipsilateral hemisphere were examined using immunoblotting.
resultsThe mixture (PGE1 22.6 nmol/kg+Li 0.5 mmol/kg) reduced infarct volume and neurological deficits induced by focal cerebral ischemia. Moreover, the mixture had a greater neuroprotective effect against cerebral ischemia compared with PGE1 or lithium alone. The mixture was effective even if it was administered 3 h after ischemia. PGE1+Li also significantly upregulated cytoprotective HSP70, GRP78, HSP60, and Bcl-2 protein levels, while decreasing p53 expression.
conclusionThese results demonstrated a PGE1+Li mixture with a therapeutic window of up to 3 h for clinical treatment of cerebral ischemia. The PGE1+Li mixture potentially exerts a protective effect after stroke through the induction of HSPs and Bcl-2 proteins.
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