Food industries produce a high amount of waste every year. These wastes represent a source of bioactive compounds to be used to produce cosmetic and nutraceutical products. In this study, the possibility to retrain food waste as a potential source of bioactive metabolites is evaluated. In particular, metabolite profiles of different parts (bulb, leaves, stems and little stems) of fennel waste were investigated by liquid chromatography coupled with mass spectrometry (LC-ESI/LTQ Orbitrap MS). To discriminate the different plant parts, a Multivariate Data Analysis approach was developed. Metabolomic analysis allowed the identification of different metabolites mainly belonging to hydroxycinnamic acid derivatives, flavonoid glycosides, flavonoid aglycons, phenolic acids, iridoid derivatives and lignans. The identification of compounds was based on retention times, accurate mass measurements, MS/MS data, exploration on specific metabolites database and comparison with data reported in the literature for F. vulgare. Moreover, the presence of different oxylipins was relieved; these metabolites for the first time were identified in fennel. Most of the metabolites identified in F. vulgare possess anti-inflammatory, antioxidant and/or immunomodulatory properties. Considering that polyphenols are described to possess antioxidant activity, spectrophotometric tests were performed to evaluate the antioxidant activity of each part of the fennel.
Foeniculum vulgare is a perennial aromatic plant whose cultivation produces large amounts of waste rich in bioactive compounds with promising anti-inflammatory activities. Nine selected metabolites were quantified through Ultra Performance Liquid Chromatography (UPLC) hyphenated to QTRAP mass spectrometry by using MRM (multiple reaction monitoring) was performed on four parts of fennel: bulb, stem, little stem, and leaf. Analysis revealed significant differences in the amount of quantified metabolites, suggesting that little stem and leaf are the most valuable parts of the waste. Phenolic acids and glycosylated flavonoids were quantified for their known possible anti-inflammatory activities; in fact, due to this reason their ability to inhibit COX-1 and COX-2 isoforms was evaluated through a fluorometric assay, resulting in specific inhibitors of COX-2 at certain concentrations. In conclusion, as the leaf of fennel may be beneficial to human health, clinical studies should include it in nutraceuticals or functional foods for human consumption.
The huge interest in the health-related properties of plant polyphenols to be applied in food and health-related sectors has brought about the development of sensitive analytical methods for metabolomic characterization. Olive leaves constitute a valuable waste rich in polyphenols with functional properties. A (HR)LC-ESI-ORBITRAP-MS analysis with a multivariate statistical analysis approach using PCA and/or PLS-DA projection methods were applied to identify polyphenols in olive leaf extracts of five varieties from the Apulia region (Italy) in two different seasonal times. A total of 26 metabolites were identified, further finding that although metabolites are common among the different cultivars, they differ in the relative intensity of each peak and within each cultivar in the two seasonal periods taken into consideration. The results of the total phenol contents showed the highest content in November for Bambina and Cima di Mola varieties (1816 and 1788 mg/100 g, respectively), followed by Coratina, Leccino, and Cima di Melfi; a similar trend was found for the antioxidant activity and RapidOxy evaluations by reaching in Bambina values of 45 mmol TE/100 g and 85 min of induction time.
IntroductionThe RNA-binding protein AU-rich-element factor-1 (AUF-1) participates to posttranscriptional regulation of genes involved in inflammation and cellular senescence, two pathogenic mechanisms of chronic obstructive pulmonary disease (COPD). Decreased AUF-1 expression was described in bronchiolar epithelium of COPD patients versus controls and in vitro cytokine- and cigarette smoke-challenged human airway epithelial cells, prompting the identification of epithelial AUF-1-targeted transcripts and function, and investigation on the mechanism of its loss.ResultsRNA immunoprecipitation-sequencing (RIP-Seq) identified, in the human airway epithelial cell line BEAS-2B, 494 AUF-1-bound mRNAs enriched in their 3’-untranslated regions for a Guanine-Cytosine (GC)-rich binding motif. AUF-1 association with selected transcripts and with a synthetic GC-rich motif were validated by biotin pulldown. AUF-1-targets’ steady-state levels were equally affected by partial or near-total AUF-1 loss induced by cytomix (TNFα/IL1β/IFNγ/10 nM each) and siRNA, respectively, with differential transcript decay rates. Cytomix-mediated decrease in AUF-1 levels in BEAS-2B and primary human small-airways epithelium (HSAEC) was replicated by treatment with the senescence- inducer compound etoposide and associated with readouts of cell-cycle arrest, increase in lysosomal damage and senescence-associated secretory phenotype (SASP) factors, and with AUF-1 transfer in extracellular vesicles, detected by transmission electron microscopy and immunoblotting. Extensive in-silico and genome ontology analysis found, consistent with AUF-1 functions, enriched RIP-Seq-derived AUF-1-targets in COPD-related pathways involved in inflammation, senescence, gene regulation and also in the public SASP proteome atlas; AUF-1 target signature was also significantly represented in multiple transcriptomic COPD databases generated from primary HSAEC, from lung tissue and from single-cell RNA-sequencing, displaying a predominant downregulation of expression.DiscussionLoss of intracellular AUF-1 may alter posttranscriptional regulation of targets particularly relevant for protection of genomic integrity and gene regulation, thus concurring to airway epithelial inflammatory responses related to oxidative stress and accelerated aging. Exosomal-associated AUF-1 may in turn preserve bound RNA targets and sustain their function, participating to spreading of inflammation and senescence to neighbouring cells.
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