Phelligridin D maintains the function of periodontal ligament cells through autophagy in glucose-induced oxidative stress
- Author:
Ji-Eun KIM
1
;
Tae-Gun KIM
;
Young-Hee LEE
;
Ho-Keun YI
Author Information
- Publication Type:Research Article
- From:Journal of Periodontal & Implant Science 2020;50(5):291-302
- CountryRepublic of Korea
- Language:English
-
Abstract:
Purpose:The objective of this study was to investigate whether phelligridin D could reduce glucose-induced oxidative stress, attenuate the resulting inflammatory response, and restore the function of human periodontal ligament cells (HPDLCs).
Methods:Primary HPDLCs were isolated from healthy human teeth and cultured. To investigate the effect of phelligridin D on glucose-induced oxidative stress, HPDLCs were treated with phelligridin D, various concentrations of glucose, and glucose oxidase.Glucose-induced oxidative stress, inflammatory molecules, osteoblast differentiation, and mineralization of the HPDLCs were measured by hydrogen peroxide (H2O2 ) generation, cellular viability, alkaline phosphatase (ALP) activity, alizarin red staining, and western blot analyses.
Results:Glucose-induced oxidative stress led to increased production of H2O2 , with negative impacts on cellular viability, ALP activity, and calcium deposition in HPDLCs. Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Phelligridin D restored all these molecules and maintained the function of HPDLCs even under glucose-induced oxidative stress.
Conclusions:This study suggests that phelligridin D reduces the inflammation that results from glucose-induced oxidative stress and restores the function of HPDLCs (e.g., osteoblast differentiation) by upregulating autophagy.
