ArticleActa pharmacologica Sinica2017
Dual anti-ischemic effects of rosmarinic acid n-butyl ester via alleviation of DAPK-p53-mediated neuronal damage and microglial inflammation.
Article in Acta pharmacologica Sinica, 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, 21 citations in OpenAlex.
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- Synthesis, characterization, and mechanistic insights into the enhanced anti-inflammatory activity of baicalin butyl ester via the PI3K-AKT pathway.Frontiers in pharmacology · 2024Article
- Neuroprotective Strategies for Stroke by Natural Products: Advances and Perspectives.Current neuropharmacology · 2023Review
- A comprehensive review of stroke-related signaling pathways and treatment in western medicine and traditional Chinese medicine.Frontiers in neuroscience · 2023Review
- Novel insight into cGAS-STING pathway in ischemic stroke: from pre- to post-disease.Frontiers in immunology · 2023Review
- Neuroprotective Effects of Sodium Butyrate through Suppressing Neuroinflammation and Modulating Antioxidant Enzymes.Neurochemical research · 2021Article
- From Preclinical Stroke Models to Humans: Polyphenols in the Prevention and Treatment of Stroke.Nutrients · 2020Review
- Death-Associated Protein Kinase 1 Phosphorylation in Neuronal Cell Death and Neurodegenerative Disease.International journal of molecular sciences · 2019Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery of efficacious anti-ischemic drugs remains a challenge. Recently we have found that rosmarinic acid n-butyl ester (RABE), a derivative of rosmarinic acid, significantly protects SH-SY5Y cells against oxygen glucose deprivation (OGD)-induced cell death. In the present study we simultaneously investigated the effects of RABE on the two key players in the pathophysiology of cerebral ischemia, ischemic neuronal damage and microglial inflammation. Pretreatment with RABE (1, 10 μmol/L) dose-dependently attenuated OGD- or H
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