ArticleJournal of molecular neuroscience : MN2020
Prostaglandin E1 Improves Cerebral Microcirculation Through Activation of Endothelial NOS and GRPCH1.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Longxue tongluo capsule enhances ischemic stroke recovery via microbiota-metabolite-gene interactions.Metabolic brain disease · 2026Article
- Photoacoustic imaging detects cerebrovascular pathological changes in sepsis.Photoacoustics · 2025Article
- Astrocyte-Derived Interleukin 11 Modulates Astrocyte-Microglia Crosstalk via Nuclear Factor-κB Signaling Pathway in Sepsis-Associated Encephalopathy.Research (Washington, D.C.) · 2025Article
- Deep and periventricular white matter hyperintensities exhibit differential metabolic profiles in arteriosclerotic cerebral small vessel disease: an untargeted metabolomics study.Frontiers in neuroscience · 2025Article
- Early prostaglandin EFrontiers in ophthalmology · 2025Article
- Citronellal improves endothelial dysfunction by affecting the stability of the GCH1 protein.Acta biochimica et biophysica Sinica · 2024Article
- The Rrp2-RpoN-RpoS pathway plays an important role in the blood-brain barrier transmigration of the Lyme disease pathogen.Infection and immunity · 2023Article
- Naringenin upregulates GTPCH1/eNOS to ameliorate high glucose-induced retinal endothelial cell injury.Experimental and therapeutic medicine · 2022Article
- Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment.Oxidative medicine and cellular longevity · 2022Review
- Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction greatly contributes to microcirculation disorder. The role of prostaglandin E1 (PGE1) in cerebral microcirculation was explored in vitro. LPS (0.5 or 1 μg/ml) was added to induce injury in human brain microvascular endothelial cells (HCMEC/D3). CCK-8 was applied to check viabilities of HCMEC/D3 before and after LPS treatment. Western blot witnessed the changes in protein expressions of inflammatory cytokines, IL-6 and TNF-α. Caspase-3/7 activity was analyzed and so were the protein expressions of pro-apoptotic gene BAX and anti-apoptotic gene Bcl-2. mRNA expressions of eNOS and GTPCH1 were evaluated by RT-qPCR. After overexpressing eNOS or GTPCH1 in LPS-induced HCMEC/D3 cells, viabilities, inflammatory cytokines, caspase-3/7 activity, and apoptosis-related genes were detected. The modulation of PGE1 in eNOS and GTPCH1 production, viability, inflammation, and apoptosis was investigated. The inhibitor of eNOS or GTPCH1 was introduced to examine impacts of eNOS or GTPCH1 could have on the PGE1 function. LPS decreased cell viabilities, eNOS and GTPCH1 expression, and promoted inflammation and apoptosis in HCMEC/D3 cells. Overexpressed eNOS or GTPCH1 promoted cell viabilities and suppressed inflammation and apoptosis. PGE1 enhanced viability and decreased inflammation and apoptosis in cells treated by LPS. PGE1 activated eNOS and GTPCH1 and inhibition of eNOS or GTPCH1 led to the attenuation of the protective functions of PGE1 in LPS-induced cells. PGE1 protected HCMEC/D3 cells from injuries induced by LPS by activation of eNOS and GTPCH1, suggesting that PGE1 might be used to help maintain cerebral microcirculation in future.
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Registered trials
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