ArticleInflammation2017
The Attenuation of 14-3-3ζ is Involved in the Caffeic Acid-Blocked Lipopolysaccharide-Stimulated Inflammatory Response in RAW264.7 Macrophages.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Exploration of the anticancer properties of Caffeic Acid in malignant mesothelioma cells.Medical oncology (Northwood, London, England) · 2025Article
- Activity-based chemical proteomics reveals caffeic acid ameliorates pentylenetetrazol-induced seizures by covalently targeting aconitate decarboxylase 1.Cell communication and signaling : CCS · 2025Article
- Comprehensive Metabolomics Profiling and Bioactivity Study ofMetabolites · 2025Article
- Caffeic acid activates mitochondrial UPR to resist pathogen infection inInfection and immunity · 2024Article
- Neutrophil membrane-mimicking nanodecoys with intrinsic anti-inflammatory properties alleviate sepsis-induced acute liver injury and lethality in a mouse endotoxemia model.Materials today. Bio · 2022Article
- Evaluation of Toxicity, Bacteriostatic, Analgesic, Anti-Inflammatory, and Antipyretic Activities of Huangqin-Honghua-Pugongying-Jinyinhua Extract.Veterinary sciences · 2021Article
- Network Pharmacology-Based Identification of Potential Targets ofBioMed research international · 2021Article
- 14-3-3ζ-TRAF5 axis governs interleukin-17A signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- trans, trans-2,4-Decadienal, a lipid peroxidation product, induces inflammatory responses via Hsp90- or 14-3-3ζ-dependent mechanisms.The Journal of nutritional biochemistry · 2020Article
- Gentiopicroside (GENT) protects against sepsis induced by lipopolysaccharide (LPS) through the NF-κB signaling pathway.Annals of translational medicine · 2019Article
- New Anti-inflammatory Flavonol Glycosides from Lindera akoensis Hayata.Molecules (Basel, Switzerland) · 2019Article
- Reversal of sorafenib resistance in hepatocellular carcinoma: epigenetically regulated disruption of 14-3-3η/hypoxia-inducible factor-1α.Cell death discovery · 2019Article
- Polyphyllin I Ameliorates Collagen-Induced Arthritis by Suppressing the Inflammation Response in Macrophages Through the NF-κB Pathway.Frontiers in immunology · 2018Article
- The Anti-Inflammatory Activity of Toonaciliatin K against Adjuvant Arthritis.BioMed research international · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation plays important roles in the initiation and progress of many diseases. Caffeic acid (CaA) is a naturally occurring hydroxycinnamic acid derivative, which shows hypotoxicity and diverse biological functions, including anti-inflammation. The molecular mechanisms involved in the CaA-inhibited inflammatory response are very complex; generally, the down-regulated phosphorylation of such important transcriptional factors, for example, nuclear factor κB (NF-κB) and signal transducers and activators of transcription-3 (STAT-3), plays an important role. Here, we found that in RAW264.7 macrophage cells, CaA blocked lipopolysaccharide (LPS)-stimulated inflammatory response by attenuating the expression of 14-3-3ζ (a phosphorylated protein regulator). Briefly, the increased expression of 14-3-3ζ was involved in the LPS-induced inflammatory response. CaA blocked the LPS-elevated 14-3-3ζ via attenuating the LPS-induced tumor necrosis factor-α (TNF-α) secretion and via enhancing the 14-3-3ζ ubiquitination. These processes inhibited the LPS-induced activation (phosphorylation) of NF-κB and STAT-3, in turn blocked the transcriptional activation of inducible NO synthase (iNOS), interleukin-6 (IL-6), and TNF-α, and finally attenuated the productions of nitric oxide (NO), IL-6, and TNF-α. By understanding a novel mechanism whereby CaA inhibited the 14-3-3ζ, our study expanded the understanding of the molecular mechanisms involved in the anti-inflammation potential induced by CaA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.