摘要
Abstract
Objective:To investigate the therapeutic effect and potential mechanism of AdipoRon on peri-implantitis of tooth.Methods:A rabbit peri-implantitis model of tooth was constructed with integrated titanium implants and divided into two groups:Control group and AdipoRon treatment group.Rabbit bone marrow mononuclear cells were induced into M2-type macrophages and were also divided into control group and administration group.CCK-8 assay was used to detect cell viability.Transwell assay was adopted to measure cell migration.The levels of interleukin-4(IL-4)and interleukin-13(IL-13)were measured by ELISA.The mRNA expression of cyclin-dependent kinase 1(CDK1),proliferating cell nuclear antigen(PCNA),Ki67,interleukin-1(IL-1),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)were detected using RT-qPCR.Western blotting was employed to determine the protein expression of AMP-activated protein kinase(AMPK)and its phosphorylated form(p-AMPK),sirtuin 1(Sirt1),inhibitor of nuclear factor-κB(IκBα)and nuclear factor-kappa B(NF-κB)p65,as well as its phosphorylated form.Results:Compared with the Control group,the AdipoRon-treated group had significantly less peri-implant inflammation and significantly increased osseous integration.The levels of IL-4 and IL-13 in periodontal tissues significantly increased.AdipoRon promoted the viability and migration of M2 type macrophages.AdipoRon significantly increased the expression levels of p-AMPK,Sirt1 and IκB,inhibited the nuclear translocation of phosphorylated NF-κB p65,and significantly decreased the mRNA levels of downstream factors IL-1,IL-6 and TNF-α in the NF-κB pathway.Conclusion:AdipoRon can promote the proliferation and migration of M2-type macrophages,possibly by activating the AMPK/Sirt1 pathway to inhibit M1 macrophage polarization,thereby improving peri-implantitis.关键词
牙种植体/炎症/巨噬细胞/AdipoRon/AMP依赖的蛋白激酶/Sirt1通路/核转录因子-κBKey words
dental implant/inflammation,macrophage/AdipoRon/AMPK/Sirt1 pathway/nuclear factor-κB分类
基础医学
