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Τετάρτη 15 Αυγούστου 2018

Effects of quercetin on human oral keratinocytes during re-epithelialization: an in vitro study

Publication date: Available online 15 August 2018

Source: Archives of Oral Biology

Author(s): Miyashaer Hujiahemaiti, Xiaolin Sun, Jing Zhou, Huixin Lv, Xue Li, Manlin Qi, Minghan Chi, Chunyan Li, Yanmin Zhou

Abstract
Background

The width of keratinized mucosa plays an important role in esthetic and functional outcomes of dental implants. Lack of keratinized mucosa may lead to poor oral hygiene and greater soft-tissue recession. This study aimed at assessing the potential of quercetin in promoting human oral keratinocyte (HOK) proliferation and re-epithelializationin vitro.

Materials and Methods

HOK were detected in the absence or presence of test substances. The Cell Counting Kit-8 was used to assess cell viability and proliferation capacity. Re-epithelization was assessed using a keratinocyte monolayer scratch assay. Cell migration was monitored via Transwell chambers. Porphyromonas gingivalis lipopolysaccharide was used to stimulate keratinocytes for mimicking the inflammatory situation. mRNA expression of inflammatory cytokines (interleukin-1beta, IL-1β and tumor necrosis factor alpha, TNF-α), cell adhesion molecules (Integrin-α6, Integrin-β4), and growth factors (transforming growth factor beta 1,TGF-β1 and transforming growth factor beta 3, TGF-β3) were estimated using RT-qPCR. Protein contents of TGF-β1 and TGF-β3 were investigated by enzyme-linked immunosorbent assay.

Results

Multiplex analysis revealed that quercetin enhances HOK proliferation via an upregulation of adhesion molecules (Integrin-α6β4). Additionally, re-epithelialization rate was significantly greater in the presence of quercetin than in the control (P < 0.01). Furthermore, 20 µM of quercetin increases both mRNA and protein levels of TGF-β3 under basal and wound conditions without affecting TGF-β1 production. Expressions of pro-inflammatory cytokines were downregulated by quercetin treatment.

Conclusion

Quercetin promotes HOKs proliferation and oral re-epithelialization in vitro.



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