BCM-95® (CURCUGREEN®), 06 Aug 2021

Anti-SASP and anti-inflammatory activity of resveratrol,
curcumin and b-caryophyllene association on human
endothelial and monocytic cells


Giulia Matacchione . Felicia Gura ̆u . Andrea Silvestrini . Mattia Tiboni . Luca Mancini . Debora Valli . Maria Rita Rippo . Rina Recchioni . Fiorella Marcheselli . Oliana Carnevali . Antonio Domenico Procopio . Luca Casettari . Fabiola Olivieri

Introduction: A challenging and promising new branch of aging-related research fields is the identification of natural compounds able to modulate the senescence associated secretory phenotype (SASP), which characterizes senescent cells and can contribute to fuel the inflammaging.

Methods: We investigated both the anti-SASP and anti-inflammatory activities of a nutritional supplement, namely FenoxidolTM, composed of turmeric extract bioCurcumin (bCUR), Polydatin (the natural glycosylated precursor of Resveratrol-RSV), and liposomal b-caryophyllene (BCP), in two human cellular models, such as the primary endothelial cell line, HUVECs and the monocytic cell line, THP-1. Replicative and Doxorubicin-induced senescent HUVECs, both chosen as cellular models of SASP, and lipopolysaccharides (LPS)-stimulated THP-1, selected as a model of the inflammatory response, were treated with the three single natural compounds or with a combination of them (MIX).

Result: In both senescent HUVEC models, MIX treatment significantly reduced IL-1b and IL-6 expression levels and p16ink4a protein, and also increased SIRT1 protein level, as well as downregulated miR-146a and miR-21 expression, two of the so-called inflamma-miRNAs, more effectively than the single compounds. In THP-1 cells stimulated with LPS, the MIX showed a significant effect in decreasing IL-1b, IL-6, TNF-a, and miR-146a expression levels and Caspase-1 activation, in association with an up-regulation of SIRT1 protein, compared to the single compounds. Overall, our results suggest that the three analysed compounds can have a combined effect in restraining SASP in senescent HUVECs as well as the inflammatory response in LPS-stimulated THP-1 cells.



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