Sitagliptin inhibits lipopolysaccharide-induced inflammatory response in human gingival fibroblasts by blocking nuclear factor-κB signaling pathway.
- Author:
Xiang LIU
1
;
Wen-Yan KANG
1
;
Ling-Ling SHANG
1
;
Shao-Hua GE
1
Author Information
- Publication Type:Journal Article
- Keywords: Sitagliptin; human gingival fibroblasts; inflammation; lipopolysaccharide; nuclear factor-κB
- MeSH: Fibroblasts; Gingiva/metabolism*; Humans; Lipopolysaccharides; NF-kappa B/metabolism*; Signal Transduction; Sitagliptin Phosphate
- From: West China Journal of Stomatology 2021;39(2):153-163
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:This study was performed to clarify the effects of sitagliptin on
METHODS:Healthy gingival samples were collected from the donors. HGFs were isolated with enzymic digestion method and identified. The effects of LPS and sitagliptin on cell viability were detected by cell-counting kit-8 (CCK8). The mRNA levels of inflammatory cytokines, namely, interleukin (IL)-6, IL-8, C-C motif ligand 2 (CCL2), and superoxide dismutase 2 (SOD2), were evaluated by quantity real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immune sorbent assay (ELISA) was used to measure the secretion protein levels of IL-6, IL-8, and CCL2. Western blot analysis was used to further investigate the activation of nuclear factor (NF)-κB signaling pathway. The effect of NF-κB pathway inhibitor BAY11-7082 on LPS-induced HGF inflammatory cytokines at the gene level was verified by qRT-PCR.
RESULTS:Low concentrations of sitagliptin (0.1, 0.25, and 0.5 µmol·L
CONCLUSIONS:Sitagliptin could significantly inhibit LPS-induced HGF inflammatory response by blocking the NF-κB signaling pathway activation.
