ArticleMolecular medicine reports2017
Lipo‑prostaglandin E1 modifies cognitive impairment in rats with vascular cognitive impairment by promoting angiogenesis via the VEGF/VEGFR pathway.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Da chuanxiong formula improves vascular remodeling via promoting angiogenesis and vasodilation mediated by PI3K/Akt/eNOS signaling.Metabolic brain disease · 2026Article
- Endogenous neuroprotection in vascular cognitive impairment and dementia.EBioMedicine · 2026Review
- Vasoactive neuropeptide dysregulation: A novel mechanism of microvascular dysfunction in vascular cognitive impairment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Upregulation of VEGFA through the adenosine A2A receptor is a crucial pathway for inhibiting pericyte apoptosis in chronic cerebral hypoperfusion.Scientific reports · 2025Article
- Effects of PGE1 on the ERS pathway in neonatal rats with hyperoxic lung injury.Pediatric research · 2025Article
- Baicalein ameliorates cognitive decline induced by chronic cerebral hypoperfusion through the SIRT1-mediated Notch1 pathway to improve angiogenesis and suppress neuroinflammation.Frontiers in aging neuroscience · 2025Article
- Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics.Frontiers in neuroscience · 2019Article
- Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathological mechanism of vascular cognitive impairment (VCI) involves ischemic lesions in the hippocampus. Prostaglandin E1 (PGE1) serves roles in the promotion of vascular endothelial growth factor (VEGF) expression, angiogenesis and enhances blood flow to ischemic regions. However, the effect of PGE1 on cognitive function in VCI rats and the underlying mechanism are unknown. In the current study, learning and memory function in VCI rats treated by lipo‑PGE1 injection was assessed through Morris Water Maze test. Furthermore, the histological alterations, blood vessel numbers in the hippocampal CA1 region and relative VEGF protein and mRNA expression were researched. The results confirmed that VCI rats treated with lipo‑PGE1 presented improved cognitive function, less neuronal cell loss, a greater number of blood vessels in the hippocampal region and higher VEGF protein and mRNA expression. However, the role of lipo‑PGE1 in VCI rats can be inhibited by SU5416 (a specific VEGFR2 antagonist). The results indicated that lipo‑PGE1 may alleviate cognitive deficits in VCI rats. The underlying mechanism may be associated with angiogenesis promoted by lipo‑PGE1, which may involve the VEGF/VEGFR pathway. These findings may have therapeutic implications for cognitive impairment induced by hypoperfusion or chronic ischemic lesions.
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