PPARγ Regulating NF-κB Signaling Pathway in Lipopolysaccharide-induced Human Periodontal Ligament Cells.

doi:10.13701/j.cnki.kqyxyj.2017.07.003

Abstract

Abstract: Objective: To explore the mechanism of PPARγ in periodontitis. Methods: Human periodontal ligament cells (hPDLCs) were cultured in tissue blocks. Cells were divided into four groups. Group A: normal control group; Group B:LPS group; Group C: rosiglitazone control group; Group D: rosiglitazone group. Expression of PPARγ and NF-κB p65 were detected by western blot. Cell immunofluorescence was employed to determine the location of NF-κB p65 in hPDLCs. RNA expression of IL-1β and TNF-α was detected by realtime PCR and protein expression was detected by ELISA. Results: After stimulated by LPS, protein expression of PPARγ decreased and NF-κB p65 increased in cellular nuclei. Moreover, the RNA and protein expression of IL-1β and TNF-α were significantly increased. When stimulated by LPS and rosiglitazone, protein expression of PPARγ increased and NF-κB p65 decreased in cellular nuclei, and the RNA and protein expression of IL-1β and TNF-α significantly decreased.These difference were statistically significant (P<0.01). Conclusion: PPARγ inhibits lipopolysaccharide-induced RNA expression and protein secretion of cytokines in human periodontal ligament cells via downregulation of NF-κB signaling pathway, and then regulate inflammatory responses in periodontal disease.

Key words: PPARγ, Rosiglitazone , Periodontal ligament cells, Cytokines , NF- κB signaling pathway

CLC Number:

R781.4

YANG Fang, CHEN Ming-yue, HU Ying-ying, WANG Chang-ning.. PPARγ Regulating NF-κB Signaling Pathway in Lipopolysaccharide-induced Human Periodontal Ligament Cells.[J]. Journal of Oral Science Research, 2017, 33(7): 698-702.

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