[1]张 晶,贾翠楠,何 冰,等.金丝桃苷抑制Toll样受体4/髓样分化因子88/核因子-κB信号通路减轻牙周炎大鼠牙周组织损伤实验研究[J].陕西医学杂志,2023,52(11):1463-1467,1472.[doi:DOI:10.3969/j.issn.1000-7377.2023.11.003]
　ZHANG Jing,JIA Cuinan,HE Bing,et al.Hyperoside inhibits TLR4/MyD88/NF-κB signaling pathway to reduce periodontal tissue damage in rats with periodontitis[J].,2023,52(11):1463-1467,1472.[doi:DOI:10.3969/j.issn.1000-7377.2023.11.003]
点击复制

金丝桃苷抑制Toll样受体4/髓样分化因子88/核因子-κB信号通路减轻牙周炎大鼠牙周组织损伤实验研究
分享到：

《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
52
期数:
2023年11期
页码:
1463-1467,1472
栏目:
基础研究
出版日期:
2023-11-05

文章信息/Info

Title:
Hyperoside inhibits TLR4/MyD88/NF-κB signaling pathway to reduce periodontal tissue damage in rats with periodontitis
作者:
张 晶; 贾翠楠; 何 冰; 李彬琦; 巩兰平
(邯郸市中心医院口腔科,河北 邯郸 056000)
Author(s):
ZHANG Jing; JIA Cuinan; HE Bing; LI Binqi; GONG Lanping
(Department of Stomatology,Handan Central Hospital,Handan 056000,China)
关键词:
金丝桃苷;  Toll样受体4/髓样分化因子88/核因子-κB信号通路;  牙周炎;  牙周组织;  损伤;  炎性反应
Keywords:
Hyperoside;  Toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-κB signaling pathway;  Periodontitis;  Periodontal tissue;  Damage;  Inflammatory response
分类号:
R 781.42
DOI:
DOI:10.3969/j.issn.1000-7377.2023.11.003
文献标志码:
A
摘要:
目的:探究金丝桃苷调控Toll样受体4(TLR4)/髓样分化因子88(MyD88)/核因子-κB(NF-κB)信号通路对牙周炎大鼠牙周组织损伤的影响。方法:构建牙周炎大鼠模型,建模成功大鼠随机分为模型组、金丝桃苷(30 mg/kg)组、金丝桃苷(30 mg/kg)+TLR4激活剂(脂多糖,0.4 mg/kg)组,每组15只,另取15只健康大鼠作为对照组,建模结束后,各组大鼠按对应方式给药,1次/d,连续4周。HE染色及抗酒石酸酸性磷酸酶染色分别观察各组大鼠牙周组织病理变化及破骨细胞数量; ELISA法检测各组大鼠血清骨保护素(OPG)、NF-κB受体活化因子配体(RANKL)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)水平; 荧光定量PCR法检测各组大鼠牙周组织TLR4、MyD88、NF-κB mRNA表达水平; 蛋白印迹法检测各组大鼠牙周组织TLR4、MyD88、NF-κB蛋白表达水平。结果:对照组大鼠牙周组织结构正常; 与对照组相比,模型组大鼠牙周组织炎性细胞浸润明显,伴随骨吸收陷窝数量增多,牙周组织破骨细胞数量、TLR4、MyD88、NF-κB mRNA和蛋白表达水平、血清RANKL、TNF-α、IL-6水平显著升高(均P<0.05),血清OPG水平显著降低(P<0.05); 与模型组相比,金丝桃苷组大鼠牙龈上皮较完整,炎性细胞浸润程度较轻,骨吸收陷窝减少,牙周组织破骨细胞数量、TLR4、MyD88、NF-κB mRNA和蛋白表达水平、血清RANKL、TNF-α、IL-6水平显著降低(均P<0.05),血清OPG水平显著升高(P<0.05); 与金丝桃苷组相比,金丝桃苷+TLR4激活剂组大鼠牙周组织炎性细胞浸润程度加深,骨吸收陷窝增多,牙周组织破骨细胞数量、TLR4、MyD88、NF-κB mRNA和蛋白表达水平、血清RANKL、TNF-α、IL-6水平显著升高(均P<0.05),血清OPG水平显著降低(P<0.05)。结论:金丝桃苷可缓解牙周炎大鼠牙周组织损伤,抑制大鼠炎性反应,其机制与抑制TLR4/MyD88/NF-κB信号通路有关。
Abstract:
Objective:To investigate the effect of hyperoside on periodontal tissue damage in rats with periodontitis by regulating Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)signaling pathway.Methods:The rat model of periodontitis was established,and the successful model rats were randomly divided into model group,hyperoside(30 mg/kg)group,and hyperoside(30 mg/kg)+TLR4 activator(lipopolysaccharide,0.4 mg/kg)group,with 15 in each group.Another 15 healthy rats were selected as control group.Following the modeling procedure,the corresponding method was administered to each group of rats once daily for a duration of 4 weeks.HE staining and tartrate-resistant acid phosphatase staining were used to observe the pathological changes of periodontal tissue and the number of osteoclasts in each group.The serum levels of osteoprotegerin(OPG),receptor activator of NF-κB ligand(RANKL),tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)were detected by ELISA.The mRNA levels of TLR4,MyD88 and NF-κB in periodontal tissues were detected by fluorescence quantitative PCR method.Western blot analysis was employed to determine the protein expression levels of TLR4,MyD88,and NF-κB in periodontal tissues of rats.Results:The periodontal tissue architecture of the control group rats exhibited normalcy.Compared with control group,the model group exhibited obvious inflammatory cell infiltration in periodontal tissue,accompanied by an increase in the number of bone resorption lacunae,and the number of osteoclasts,the mRNA and protein levels of TLR4,MyD88,and NF-κB in the periodontal tissue,and the serum levels of RANKL,TNF-α,and IL-6 were significant increased,and the serum OPG level was significantly decreased(all P<0.05).Compared with model group,the gingival epithelium of the hyperoside group was more intact,the degree of inflammatory cell infiltration was lighter,and the bone resorption lacunae were reduced,the number of osteoclasts in periodontal tissue,the mRNA and protein levels of TLR4,MyD88,and NF-κB,and the serum levels of RANKL,TNF-α,and IL-6 were significantly decreased,while the serum level of OPG was significantly increased(all P<0.05).Compared with the hyperoside group,the hyperoside+TLR4 activator group had inflammatory cell infiltration in periodontal tissue,bone resorption lacunae,the number of osteoclasts,the mRNA and protein levels of TLR4,MyD88,and NF-κB in periodontal tissue,and serum RANKL,TNF-α,and IL-6 levels were significantly increased,and the serum OPG level was significantly decreased(all P<0.05).Conclusion:Hyperoside can alleviate periodontal tissue damage and inhibit inflammatory response in rats with periodontitis,and the mechanism is related to the inhibition of TLR4/MyD88/NF-κB signaling pathway.

参考文献/References:

[1] Lei F,Li M,Lin T,et al.Treatment of inflammatory bone loss in periodontitis by stem cell-derived exosomes[J].Acta Biomater,2022,141(1):333-343.
[2] 李 晋.加味葛根芩连汤联合根面平整术治疗慢性牙周炎临床研究[J].陕西中医,2022,43(7):914-917.
[3] Zhao Y,Quan Y,Lei T,et al.The Role of Inflammasome NLPR3 in the Development and Therapy of Periodontitis[J].Int J Med Sci,2022,19(10):1603-1614.
[4] Xie T,Yuan J,Mei L,et al.Hyperoside ameliorates TNF-α-induced inflammation,ECM degradation and ER stress-mediated apoptosis via the SIRT1/NF-κB and Nrf2/ARE signaling pathways in vitro[J].Mol Med Rep,2022,26(2):260-277.
[5] Xu T,Wu X,Zhou Z,et al.Hyperoside ameliorates periodontitis in rats by promoting osteogenic differentiation of BMSCs via activation of the NF-κB pathway[J].Febs Open Bio,2020,10(9):1843-1855.
[6] Wei A,Song Y,Ni T,et al.Hyperoside attenuates pregnancy loss through activating autophagy and suppressing inflammation in a rat model[J].Life Sci,2020,254(1):117735-117747.
[7] 陈 晨,陈 栋,陆 珂,等.基于OPG/RANKL途径青蒿琥酯对牙周炎大鼠牙槽骨吸收的影响及抑炎作用研究[J].实用口腔医学杂志,2022,38(4):434-438.
[8] 刘国星,杜见霞,刘秀红,等.金丝桃苷对慢性心力衰竭大鼠心脏功能及自噬相关蛋白表达的影响[J].岭南心血管病杂志,2022,28(6):582-587.
[9] 黄文炼,刘鸿雁,任丽蓉,等.栀子苷抑制TLR4/RIP3/NF-κB信号通路对急性胰腺炎大鼠肠损伤的影响[J].四川医学,2022,43(12):1178-1184.
[10] Mathew JE,Jacob JJ,Kalra S.Periodontitis management in diabetes care[J].J Pak Med Assoc,2021,71(8):2097-2099.
[11] Parsegian K,Randall D,Curtis M,et al.Association between periodontitis and chronic kidney disease[J].Periodontol,2022,89(1):114-124.
[12] 刘 阳,高秀秋.复方米诺环素奥硝唑温敏凝胶治疗老年慢性牙周炎疗效及对龈沟液中人类刺猬因子蛋白、基质金属蛋白酶-8水平的影响[J].陕西医学杂志,2021,50(1):82-85.
[13] Wei Y,Fu J,Wu W,et al.Quercetin prevents oxidative stress-induced injury of periodontal ligament cells and alveolar bone loss in periodontitis[J].Drug Des Devel Ther,2021,15(1):3509-3522.
[14] Cafferata EA,Castro-Saavedra S,Fuentes-Barros G,et al.Boldine inhibits the alveolar bone resorption during ligature-induced periodontitis by modulating the Th17/Treg imbalance[J].J Periodontol,2021,92(1):123-136.
[15] Ateeq H,Zia A,Husain Q,et al.Effect of inflammation on bones in diabetic patients with periodontitis via RANKL/OPG system:A review[J].J Diabetes Metab Disord,2022,21(1):1003-1009.
[16] Zhou YQ,Zhao YT,Zhao XY,et al.Hyperoside suppresses lipopolysaccharide-induced inflammation and apoptosis in human umbilical vein endothelial cells[J].Curr Med Sci,2018,38(2):222-228.
[17] 王西彬,左瑞庭.金丝桃苷对IL-1β诱导的小鼠骶髂关节软骨细胞损伤的影响[J].中成药,2021,43(2):369-373.
[18] 孟 宏,王桂青,杜竹君.西红花苷通过调控TLR4/MyD88/NF-κB通路改善糖尿病大鼠视网膜病变机制研究[J].陕西医学杂志,2023,52(5):531-535,540.
[19] 文小竹,谭光波,朴金安.补肺健脾益肾方对COPD模型大鼠TLR4/MyD88/NF-κB通路相关因子的影响[J].陕西中医,2021,42(9):1163-1166.
[20] Ali M,Yang F,Jansen JA,et al.Lipoxin suppresses inflammation via the TLR4/MyD88/NF-κB pathway in periodontal ligament cells[J].Oral Dis,2020,26(2):429-438.(收稿:2023-04-28)

备注/Memo

备注/Memo:
基金项目:河北省医学科学研究计划项目(20220551)
更新日期/Last Update: 2023-11-06