Quercetin protects human oral keratinocytes from lipopolysaccharide-induced injury by downregulating microRNA-22.
Apoptosis
/ drug effects
Cells, Cultured
Down-Regulation
/ drug effects
Humans
Janus Kinase 1
/ metabolism
Keratinocytes
/ drug effects
Lipopolysaccharides
/ pharmacology
MicroRNAs
Phosphatidylinositol 3-Kinases
/ metabolism
Protective Agents
/ pharmacology
Proto-Oncogene Proteins c-akt
/ metabolism
Quercetin
/ pharmacology
STAT3 Transcription Factor
/ metabolism
JAK1/STAT3
PI3K/AKT
Quercetin
apoptosis
cell viability
human oral keratinocytes
Journal
Human & experimental toxicology
ISSN: 1477-0903
Titre abrégé: Hum Exp Toxicol
Pays: England
ID NLM: 9004560
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
pubmed:
25
4
2020
medline:
10
4
2021
entrez:
25
4
2020
Statut:
ppublish
Résumé
Quercetin exerts anti-inflammatory effects, but whether it can benefit patients with the chronic inflammatory disease of oral lichen planus (OLP), which is a common chronic mucocutaneous disorder with an immune-mediated pathogenesis, is unclear. The present research examined the impacts of quercetin in a cell-based OLP model in which human oral keratinocytes (HOKs) were treated with lipopolysaccharide (LPS). Effects of quercetin on viability, proliferation, and apoptosis of HOKs were assessed using the Cell Counting Kit-8 assay, Western blotting, and flow cytometry, respectively. Effects of treatment on levels of microRNA-22 (miR-22) were measured using stem-loop reverse transcription polymerase chain reaction, while levels of proteins and phosphorylation in the PI3K/AKT and JAK1/STAT3 cascades were analyzed by Western blot. Quercetin mitigated LPS-induced reduction in HOK viability and elevation of apoptosis. It also weakened LPS-induced upregulation of miR-22. Quercetin treatment led to significantly higher levels of p-PI3K, p-AKT, p-JAK1, and p-STAT3. These effects of quercetin were enhanced when miR-22 was knocked down and partly reversed when miR-22 was overexpressed. Quercetin can mitigate LPS-induced injury in HOKs by downregulating miR-22, thereby activating PI3K/AKT and JAK1/STAT3 cascades.
Sections du résumé
BACKGROUND
BACKGROUND
Quercetin exerts anti-inflammatory effects, but whether it can benefit patients with the chronic inflammatory disease of oral lichen planus (OLP), which is a common chronic mucocutaneous disorder with an immune-mediated pathogenesis, is unclear. The present research examined the impacts of quercetin in a cell-based OLP model in which human oral keratinocytes (HOKs) were treated with lipopolysaccharide (LPS).
METHODS
METHODS
Effects of quercetin on viability, proliferation, and apoptosis of HOKs were assessed using the Cell Counting Kit-8 assay, Western blotting, and flow cytometry, respectively. Effects of treatment on levels of microRNA-22 (miR-22) were measured using stem-loop reverse transcription polymerase chain reaction, while levels of proteins and phosphorylation in the PI3K/AKT and JAK1/STAT3 cascades were analyzed by Western blot.
RESULTS
RESULTS
Quercetin mitigated LPS-induced reduction in HOK viability and elevation of apoptosis. It also weakened LPS-induced upregulation of miR-22. Quercetin treatment led to significantly higher levels of p-PI3K, p-AKT, p-JAK1, and p-STAT3. These effects of quercetin were enhanced when miR-22 was knocked down and partly reversed when miR-22 was overexpressed.
CONCLUSION
CONCLUSIONS
Quercetin can mitigate LPS-induced injury in HOKs by downregulating miR-22, thereby activating PI3K/AKT and JAK1/STAT3 cascades.
Identifiants
pubmed: 32329368
doi: 10.1177/0960327120918291
doi:
Substances chimiques
Lipopolysaccharides
0
MIRN22 microRNA, human
0
MicroRNAs
0
Protective Agents
0
STAT3 Transcription Factor
0
STAT3 protein, human
0
Quercetin
9IKM0I5T1E
JAK1 protein, human
EC 2.7.10.2
Janus Kinase 1
EC 2.7.10.2
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM