辛伐他汀经AMPK激活ILC2s免疫调节治疗牙周炎的实验研究

Chronic periodontitis can cause irreversible inflammatory destruction of periodontal tissue, posing a significant threat to the patient's health. The autoimmune response is closely related to the progress and severity of periodontitis. Therefore, it is the key of treatment to adjust the body's immunity to realize the anti-inflammation / repair of periodontal tissue. ILCs is an important part of the body's immune system, little research has been done on the relationship between periodontitis and ILCs. For the first time, applicants isolated ILCs in a periodontitis model and found that the number of ILC2s in local inflammatory tissues and the secretion of factors increased, and this change was more pronounced in AMPK KO mice. It is known that simvastatin can effectively promote the anti-inflammation and regeneration processes of periodontitis, the applicant found that this may associated with the activation of AMPK / NF-κB pathway. However, it is not yet clear whether there is a link between simvastatin and ILC2s immunoregulation during the correction of periodontitis. The project holds the drug-mediated periodontitis immunomodulation therapy as the main line of research, focuses on the ILC2s immunomodulatory effect of simvastatin, explores the molecular regulatory mechanisms of AMPK on this effect, discover the network relationship and regulation mechanism of the regeneration / inflammation / immune stages of periodontal tissue through in vitro and in vivo experiments to provides new ideas and strategies for the realization of immunomodulatory treatment of periodontitis.

慢性牙周炎可导致牙周组织不可逆的炎性破坏，给患者健康带来巨大威胁。自身免疫应答与牙周炎的进展和严重程度密切相关，因此通过药物调节机体免疫以实现牙周组织的抑炎/修复是治疗的关键。ILCs是机体免疫系统的重要组成部分，其与牙周炎的关系研究甚少。申请人首次在牙周炎模型中分离得到ILCs，并发现局部炎症组织内ILC2s的数目增多、因子分泌功能增强，且在AMPK KO鼠中这种变化更为显著。现已知辛伐他汀可有效促进牙周炎的抑炎和再生，申请人发现其作用和激活AMPK/NF-κB通路有关，但尚不明确辛伐他汀与ILC2s免疫调节之间是否存在联系。本项目以药物介导牙周炎的免疫调节治疗为研究主线，围绕辛伐他汀的ILC2s免疫调节作用这一核心问题，深入探讨AMPK对该特性的分子调节机制，通过体内体外实验探讨牙周组织再生/炎症/免疫之间的网络关系及变化规律，为实现牙周炎的免疫调节治疗提供新的思路和策略.

慢性牙周炎可导致牙周组织不可逆的炎性破坏，给患者的局部和全身健康带来巨大威胁。自身免疫应答与牙周炎的进展和严重程度密切相关，因此通过药物调节机体免疫以实现牙周组织的抑炎/修复是治疗的关键。ILCs是机体免疫系统的重要组成部分，其与牙周炎的关系研究甚少。申请人在牙周炎模型中分离得到ILCs，并发现局部炎症组织内ILC2s的数目增多、因子分泌功能增强。体内体外试验发现有效浓度的辛伐他汀可有效促进牙周炎的抑炎和再生，其作用与激活AMPK/NF-κB通路有关。本项目以药物介导牙周炎的免疫调节治疗为研究主线，围绕辛伐他汀的ILCs免疫调节作用这一核心问题，深入探讨AMPK对该特性的分子调节机制，通过体内体外实验探讨牙周组织再生/炎症/免疫之间的网络关系及变化规律，为实现牙周炎的免疫调节治疗提供新的思路和策略。