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Copyright (c) 2022 Libo Wu, Gan Huang, Longkun Liu, Qin Zhang, Jie Hu, Shuting Pan
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Effects of High-Glucose Environment on Periodontal Ligament Cell Proliferation and Apoptosis via NF-κB Signaling Pathway
Corresponding Author(s) : Shuting Pan
Cellular and Molecular Biology,
Vol. 68 No. 10: Issue 10
Abstract
The purpose of this study was to discuss the function of the high-glucose environment on the periodontal ligament cell (PDLC) proliferation and apoptosis and the action mechanism of the NF-κB signaling pathway in this process. For this purpose, the human PDLCs were cultured in vitro using 5.5 mM (control group)/24.0 mM glucose (HG group) of glucose and 10 μM of QNZ+24.0 mM of glucose (HG+QNZ), respectively, and the cell proliferation level was checked through CCK-8 assay. TUNEL assay was used to perform cell apoptosis. ELISA was utilized to explore the secretion levels of the proinflammatory factors interleukin (IL)-1β and IL-6 proteins. The p65 and p50 proteins level were tested via the Western blotting (WB) assay. Results showed that in comparison with the control group, 24.0 mM of glucose could significantly decrease the proliferation ability of the PDLCs (p<0.01), cause cell apoptosis (p<0.05) and promote the secretion of IL-6 and IL-1β (p<0.05). The expressions of p65 and p50 proteins were up-regulated obviously in the high-glucose environment (p<0.05). QNZ could exert a specific inhibitory effect on the NF-κB activity to significantly down-regulate the expressions of p65 and p50 proteins (p<0.05) and reverse the effects of the high-glucose environment on the cell apoptosis and proliferation (p<0.05). In conclusion, hyper-glucose may affect PDLC proliferation and apoptosis by suppressing the NF-κB signaling pathway activity.
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