| Description: |
Prunetin mediates anti-obesity/adipogenesis effects by suppressing obesity-related transcription through a feedback mechanism that regulates the expression of adiponectin, adipoR1, adipoR2, and AMPK. Prunetin and biochanin A are potent reducers of NF-κB and ERK activation, zonula occludens 1 tyrosine phosphorylation, and metalloproteinase-mediated shedding activity, which may account for the barrier-improving ability of these isoflavones. |
| In vitro: |
| Tuberc Respir Dis (Seoul). 2013 Nov;75(5):205-9. | | Effect of Prunetin on TNF-α-Induced MUC5AC Mucin Gene Expression, Production, Degradation of IκB and Translocation of NF-κB p65 in Human Airway Epithelial Cells.[Pubmed: 24348668] | We investigated whether prunetin significantly affects tumor necrosis factor-α (TNF-α)-induced MUC5AC mucin gene expression, production, inhibitory kappa B (IκB) degradation and nuclear factor kappa B (NF-κB) p65 translocation in human airway epithelial cells.
METHODS AND RESULTS:
Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-α for 24 hours or the indicated periods. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The effect of prunetin on TNF-α-induced degradation of IκB and translocation of NF-κB p65 was investigated by western blot analysis.
We found that incubation of NCI-H292 cells with prunetin significantly inhibited mucin production and down-regulated the MUC5AC gene expression induced by TNF-α. Prunetin inhibited TNF-α-induced degradation of IκB and translocation of NF-κB p65.
CONCLUSIONS:
This result suggests that prunetin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-κB signaling pathway. | | Free Radic Biol Med. 2014 May;70:255-64. | | Biochanin A and prunetin improve epithelial barrier function in intestinal CaCo-2 cells via downregulation of ERK, NF-κB, and tyrosine phosphorylation.[Pubmed: 24631489] | The single-layered gut epithelium represents the primary line of defense against environmental stressors; thereby monolayer integrity and tightness are essentially required to maintain gut health and function. To date only a few plant-derived phytochemicals have been described as affecting intestinal barrier function.
CONCLUSIONS:
We investigated the impact of 28 secondary plant compounds on the barrier function of intestinal epithelial CaCo-2/TC-7 cells via transepithelial electrical resistance (TEER) measurements. Apart from genistein, the compounds that had the biggest effect in the TEER measurements were biochanin A and prunetin. These isoflavones improved barrier tightness by 36 and 60%, respectively, compared to the untreated control. Furthermore, both isoflavones significantly attenuated TNFα-dependent barrier disruption, thereby maintaining a high barrier resistance comparable to nonstressed cells. In docking analyses exploring the putative interaction with the tyrosine kinase EGFR, these novel modulators of barrier tightness showed very similar values compared to the known tyrosine kinase inhibitor genistein.
CONCLUSIONS:
Both biochanin A and prunetin were also identified as potent reducers of NF-κB and ERK activation, zonula occludens 1 tyrosine phosphorylation, and metalloproteinase-mediated shedding activity, which may account for the barrier-improving ability of these isoflavones. | | Biomed Pharmacother . 2018 Oct;106:1469-1477. | | Prunetin inhibits lipopolysaccharide-induced inflammatory cytokine production and MUC5AC expression by inactivating the TLR4/MyD88 pathway in human nasal epithelial cells[Pubmed: 30119221] | | Abstract
Allergic rhinitis (AR) is a chronic upper respiratory disorder characterized by inflammation of the nasal mucosa. Prunetin is an O-methylated isoflavone, which has been found to possess anti-inflammatory activity. The aim of the current study was to evaluate the effect of prunetin on inflammatory cytokine and mucus production and its underlying mechanism in nasal epithelial cells. Results showed that treatment with prunetin (10, 30, and 50 μM) inhibited lipopolysaccharide (LPS)-induced expression and secretion of interleukin (IL)-6, IL-8, and mucin 5 AC (MUC5 AC) in RPMI2650 cells, and attenuated the effect of LPS on toll-like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) expression. TAK-242 (an inhibitor of TLR4) treatment or TLR4 knockdown attenuated LPS-induced expression and secretion of IL-6, IL-8 and MUC5 AC. In conclusion, prunetin inhibited LPS-induced inflammatory cytokine production and MUC5 AC expression and secretion by inactivating the TLR4/MyD88 pathway in human nasal epithelial cells. These results suggested that prunetin might be a useful agent in the treatment of AR.
Keywords: Allergic rhinitis; Inflammatory cytokine; MUC5AC; Prunetin; TLR4/MyD88 pathway. |
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