普鲁士蓝纳米颗粒通过TLR4/MyD88/NF-κB通路抑制小鼠实验性牙周炎的组织学研究  

Histological study of Prussian blue nanoparticles inhibiting experimental pe-riodontitis in mice via TLR4/MyD88/NF-κB pathway

作　　者：崔兵 李佳轩 孙冬梅 陈小娇 孙铭 刘培红[1] CUI Bing;LI Jia-xuan;SUN Dong-mei;CHEN Xiao-jiao;SUN Ming;LIU Pei-hong(Department of Periodontics,The First Afiliated Hospital of Harbin Medical University,Harbin Medical University,Harbin 150001,China)

机构地区：[1]哈尔滨医科大学附属第一医院口腔牙周科,黑龙江哈尔滨150001

出　　处：《哈尔滨医科大学学报》2024年第6期571-575,582,共6页Journal of Harbin Medical University

摘　　要：目的探讨局部应用普鲁士蓝纳米颗粒(Prussian blue nanoparticles,PB NPs)能否治疗小鼠实验性牙周炎及其可能机制。方法小鼠24只随机分为3组,分别为空白对照组、给药组和牙周炎组(n=8),后两组小鼠采用丝线结扎法建立实验性牙周炎模型,模型建立成功后分别于局部炎症牙周组织的龈沟处注入1 mg/mL的PB NPs溶液(给药组)10μL和等量的PBS缓冲液(牙周炎组),空白对照组不做任何处理;染色观察各组小鼠牙周组织学变化。结果苏木精-伊红(hematoxylin eosin,HE)染色、Masson三色染色及定量分析结果显示,给药组小鼠牙周组织的炎症情况较牙周炎组有明显的改善且附着水平丧失程度减少(P<0.0001);抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)染色显示,给药组小鼠局部破骨细胞浸润程度显著减轻;免疫组化(immumohistochemistry,IHC)染色显示,给药组小鼠局部TLR4、MyD88及p-NF-κB-p65的表达水平较牙周炎组有所降低。结论PB NPs通过抑制破骨缓解小鼠实验性牙周炎,可能与PB NPs抑制TLR4/MyD88/NF-κB信号通路有关。Objective To explores whether the local application of Prussian blue nanoparticles(PB NPs)can treat experimental periodontitis in mice and investigates its potential mecha-nisms.Methods Twenty-four mice were randomly divided into three groups,blank control group,medication group and periodontitis group(n=8),the mice in latter two groups were used to establish the experimental periodontitis model with silk ligature.After the successful es-tablishment of the model,10μL of 1 mg/mL PB NPs solution(medication group)and equal a-mount of PBS buffer(periodontitis group)were injected into the gingival sulcus.Blank control group of mice did not receive any treatment.The periodontal histological changes were ob-served.Results Hematoxylin eosin(HE)staining,Masson staining and quantitative analysis aii showed that the periodontal inflammation improved in medication group compared with the periodontitis group,and the loss of local periodontal tissue attachment level was inhibited(P<0.0001);tartrate-resistant acid phosphatase(TRAP)staining showed that the degree of local osteoclast infiltration in medication group was significantly decreased compared with the peri-odontitis group;immumohistochemistry(IHC)staining showed that the local expression levels of TLR4,MyD88 and p-NF-κB-p65 in the medication group were lower than those in the peri-odontitis group.Conclusion PB NPs could treat experimental periodontitis in mice by inhibi-ting osteoclast.It may be related to the inhibition of TLR4/MyD88/NF-κB signaling pathway by PB NPs.

关 键 词：牙周炎 普鲁士蓝 破骨细胞 TOLL样受体4 髓样分化因子88 NF-ΚB 

分 类 号：R781.42[医药卫生—口腔医学]