interleukin-8 and myricetin

Myricetin (MYR) is a common plant flavonoid with antioxidant and anticancer properties. However, the anti-aging effect of MYR on nucleus pulposus cells (NPCs) is still unknown. The study aimed to explore the effect of MYR on the senescence of NPCs.. Methyl-thiazolyl tetrazolium assay was used to detect NPCs viability. Senescence level was evaluated by senescence-associated β-galactosidase (SA-β-Gal) staining and the expression levels of P21, P16, IL-6 and IL-8. RNA-Sequencing (RNA-seq) technology was used to identify differentially expressed genes (DEGs) between hydrogen peroxide + MYR (HO + MYR) group and HO group, and Gene Ontology (GO) functional was performed to analyze DEGs. A Venn diagram was generated to screen overlapping DEGs related to aging and inflammation, and the role of the promising validated DEG was selected for further investigation by gene functional assays.. HO inhibited NPCs viability and stimulated the senescent phenotype of NPCs, whereas MYR treatment significantly reversed SA-β-gal activity in NPCs. MYR also reduced the expression of p21 and p16 and the secretion of IL-6 and IL-8 induced by HO. RNA-seq screened 421 DEGs. The GO enrichment results showed DEGs were mainly enriched in terms such as "sterol biosynthetic process". We also found SERPINE1 has the highest log2FC abs. Silence of SERPINE1 inhibited HO-induced NPCs senescence, and overexpression of SERPINE1 could limit the anti-aging effect of MYR.. MYR alleviated HO-induced senescence of NPCs by regulating SERPINE1 in vitro.

Topics: Cellular Senescence; Flavonoids; Hydrogen Peroxide; Interleukin-6; Interleukin-8; Nucleus Pulposus; Plasminogen Activator Inhibitor 1

Periodontitis that affects the underlying structures of the periodontium, including the alveolar bone, is a multifactorial disease, whose etiology involves interactions between specific bacterial species of the subgingival biofilm and the host immune components. In the present study, we investigated the effects of myricetin, a flavonol largely distributed in fruits and vegetables, on growth and virulence properties of Porphyromonas gingivalis as well as on the P. gingivalis-induced inflammatory response in host cells. Minimal inhibitory concentration values of myricetin against P. gingivalis were in the range of 62.5 to 125 μg/ml. The iron-chelating activity of myricetin may contribute to the antibacterial activity of this flavonol. Myricetin was found to attenuate the virulence of P. gingivalis by reducing the expression of genes coding for important virulence factors, including proteinases (rgpA, rgpB, and kgp) and adhesins (fimA, hagA, and hagB). Myricetin dose-dependently prevented NF-κB activation in a monocyte model. Moreover, it inhibited the secretion of IL-6, IL-8 and MMP-3 by P. gingivalis-stimulated gingival fibroblasts. In conclusion, our study brought clear evidence that the flavonol myricetin exhibits a dual action on the periodontopathogenic bacterium P. gingivalis and the inflammatory response of host cells. Therefore, myricetin holds promise as a therapeutic agent for the treatment/prevention of periodontitis.

Topics: Collagenases; Colorimetry; Fibroblasts; Flavonoids; Gene Expression Regulation, Bacterial; Gingiva; Host-Pathogen Interactions; Humans; Inflammation; Interleukin-6; Interleukin-8; Iron Chelating Agents; Matrix Metalloproteinase 3; Matrix Metalloproteinase 9; Microbial Sensitivity Tests; NF-kappa B; Periodontal Diseases; Porphyromonas gingivalis; Real-Time Polymerase Chain Reaction; RNA, Messenger; Siderophores; Virulence Factors