Effect of liraglutide on migration,proliferation,and inflammatory response of periodontal ligament fibroblasts under high glucose environment

CUI Li-juan; LI Gui-ping

doi:10.13820/j.cnki.gdyx.20232124

Abstract：Objective To investigate the effect of liraglutide on migration,proliferation,and inflammatory re-sponse of periodontal ligament fibroblasts(PDLF)under high glucose conditions.Methods PDLFs were cultured in vitro,and the culture medium was divided into low glucose control group(L group,DMEM medium containing 5.5 mmol/L glucose),high glucose group(H group,DMEM medium containing 25 mmol/L glucose),low glucose with liraglutide group(L+G group,DMEM medium containing 10 ×10-7 mmol/L liraglutide and 5.5 mmol/L glucose),and high glu-cose with liraglutide group(H+G group,DMEM medium containing 10 × 10-7 mmol/L liraglutide and 25 mmol/L glu-cose).Cell proliferation ability was determined using the CCK-8 method,cell migration ability was assessed using Tran-swell chambers,and apoptosis was measured by flow cytometry.The expression levels of Bax and Bcl-2 in PDLFs were detected by Western blot,and the expression of inflammatory factors tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,IL-6,and C reactive protein(CRP)in PDLFs was determined by enzyme-linked immunosorbent assay.Results Compared with the L group,the OD value,migration quantity,and intracellular Bcl-2 protein level of PDLFs in the H group decreased(P＜0.05);the apoptosis rate,intracellular Bax protein,and levels of TNF-α,IL-1 β,IL-6,and CRP in the culture medium increased(P＜0.05).In the H+G group,the OD value,migration quantity,and in-tracellular Bcl-2 protein level of PDLFs were significantly higher than those in the H group(P＜0.05);while the apop-tosis rate,intracellular Bax protein,and levels of TNF-α,IL-1 β,IL-6,and CRP in the culture medium were lower than those in the H group(P＜0.05).Conclusion Liraglutide can inhibit high glucose-induced apoptosis of PDLFs,promote periodontal tissue healing and repair by regulating the expression of Bax/Bcl-2,and reducing the inflammatory response.