华西口腔医学杂志2024，Vol.42Issue(3)：296-303,8.DOI:10.7518/hxkq.2024.2023352
缝隙连接蛋白43通过调控凋亡参与大鼠牙周炎相关肾损伤
Role of connexin 43 in a rat model of periodontitis-induced renal injury
摘要
Abstract
Objective This study aims to investigate the role of gap junction mediated by connexin 43(Cx43)in renal injury induced by periodontitis in rats.Methods Twelve SPF-grade Wistar male rats were divided into a control group and a periodontitis group by using a completely random number table method,with six rats in each group.The control group rats were not treated,while the periodontitis group rats were subjected to wire ligation of the neck of their bilateral maxillary first molars to construct a periodontitis model.After 8 weeks of modeling,the rats were examined for clinical indicators of the periodontium.micro-CT scanning of the maxilla reconstructed its 3D structure and analyzed the absorption of alveolar bone.Histopathological changes in periodontal and renal tissues were detected.MitoSOX red reagent was used to determine reactive oxygen species(ROS)content in renal tissues.A biochemical reagent kit was used to detect serum oxidative stress biomarkers.Real-time fluo-rescent quantitative-polymerase chain reaction(qRT-PCR)was employed to determine Cx43,nuclear factor kappa-B(NF-κB),interleukin(IL)-1β,IL-6,BCL2-Associated X(Bax),B-lymphomatoma-2 gene(Bcl-2),and Caspase-3 mRNA were determined.Western blot analysis was used to detect Cx43,NF-κB,IL-1β,Bax,Bcl-2 and Caspase-3 protein.Re-sults micro-CT 3D reconstruction showed significant bone resorption of the first molar alveolar bone in the periodonti-tis group rats and decreased height of the alveolar ridge.The distance from the enamel cementum boundary to the top of the alveolar ridge in the periodontitis group was significantly higher than that inthe control group.The histopathological results showed a large number of inflammatory cells that infiltrated the periodontal tissue of the periodontitis group,and the alveolar bone was significantly absorbed.Rats in the periodontitis group also exhibited mild thickening of the glomer-ular basement membrane,dilation of the Bowman's capsule,and destruction of the brush-like edge of the renal tubules in the renal tissue.The MitoSOX red staining results showed a significant increase in ROS content in the renal tissue of the periodontitis group.The biochemical test results showed that the levels of superoxide dismutase and glutathione in the serum of rats with periodontitis decreased,while that of malondialdehyde increased.The results of qRT-PCR and Western blot showed that the expression levels of Cx43,IL-1β,IL-6,Bax,Caspase-3 mRNA and Cx43,IL-1β,NF-κB,Bax,Caspase-3 proteins in the periodontitis group significantly increased compared with those in the control group,while the expression levels of Bcl-2 mRNA and protein decreased.Conclusion Periodontitis may activate NF-κB sig-naling molecules by upregulating the expression of Cx43 in rat kidney tissues,leading to increased levels of inflamma-tion and apoptosis and ultimately inducing kidney injury.关键词
牙周炎/肾损伤/缝隙连接蛋白43/大鼠/凋亡Key words
periodontitis/renal injury/connexin 43/rat/apoptosis分类
医药卫生引用本文复制引用
辛雨,傅若冰,辛禧瑞,商雅琦,刘歆婵,于维先..缝隙连接蛋白43通过调控凋亡参与大鼠牙周炎相关肾损伤[J].华西口腔医学杂志,2024,42(3):296-303,8.基金项目
International Cooperation Project of Jilin Provincial Department of Science and Technology(20220402-069GH)吉林省科技厅国际合作项目(20220402069GH) （20220402-069GH）
