ArticleMolecular medicine reports2021
Bakkenolide‑IIIa ameliorates lipopolysaccharide‑induced inflammatory injury in human umbilical vein endothelial cells by upregulating LINC00294.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- GWAS for Periodontitis Phenotypes Using Multi-Ancestry All of Us Research Platform.medRxiv : the preprint server for health sciences · 2025Article
- METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression.Heliyon · 2023Article
- LPI-EnEDT: an ensemble framework with extra tree and decision tree classifiers for imbalanced lncRNA-protein interaction data classification.BioData mining · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
Inflammation, which causes injury to vascular endothelial cells, is one of the major factors associated with atherosclerosis (AS); therefore, inhibition of endothelial inflammation is a key step toward preventing AS. The present study aimed to investigate the effects of bakkenolide‑IIIa (Bak‑IIIa), an important active component of bakkenolides, on endothelial inflammation, as well as the mechanisms underlying such effects. Lipopolysaccharide (LPS)‑damaged human umbilical vein endothelial cells (HUVECs) were treated with Bak‑IIIa. The results of the MTT assay and enzyme‑linked immunosorbent assay indicated that Bak‑IIIa significantly alleviated survival inhibition, and decreased the levels of LPS‑induced TNF‑α, interleukin (IL)‑1β, IL‑8, and IL‑6. Furthermore, long noncoding RNA (lncRNA) microarray analyses revealed 70 differentially expressed lncRNAs (DELs) in LPS‑damaged HUVECs treated with Bak‑IIIa. lncRNA target prediction results revealed that 44 DELs had 52
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