炎症因子通过核因子κB通路促进口腔鳞状细胞癌转移的体外研究

目的 探讨炎症因子与核因子κB(nuclear factor kappa B,NF-κB)信号转导通路在口腔鳞状细胞癌转移中的意义.方法 应用口腔鳞状细胞癌低转移细胞系Tca8113和高转移细胞系Tb为研究对象,通过蛋白质印迹法和荧光素酶报告基因法检测口腔鳞状细胞癌细胞系中NF-κB通路活性.用NF-κB抑制因子α(inhibitor of kappa B alpha,IκBa)抑制质粒第32、36位丝氨酸磷酸化位点被丙氨酸替代的质粒(pBabe-SR-IκBa)和NF-κB通路抑制剂吡咯烷二硫代氨基甲酸盐(pyrolidinedithiecar bamate,PDTC)抑制信号转导通路活性,并用侵袭小室实验(TransweH)检测口腔鳞状细胞癌高转移系Tb细胞侵袭能力的变化.此外,通过酶联免疫吸附法检测pBabe-SR-IκBα和PDTC抑制信号转导通路后,肿瘤坏死因子α(tumor necrosis factor-alpha,TNF-α)、白介素(IL)-1a、IL-6、IL-8和粒-巨噬细胞集落刺激因子(granulocyte-macrophage colony stimulating factor,GM-CSF)等炎症因子的分泌.结果 蛋白质印迹法检测显示:高转移Tb细胞中磷酸化IκBα和磷酸化p65的表达量明显高于低转移细胞系Tea8113,分别为Tea8113细胞的3.19倍和6.81倍.荧光素酶(luciferase)报告基因结果显示,Tb细胞NF-κB的启动子活性为Tca8113的2.12倍(P<0.01),并对TNF-α更为敏感.转染pBabe-SR-IκBα和应用PDTC抑制NF-κB通路后,对Tb细胞的体外侵袭能力抑制率分别为21.9%和69.3%.此外,酶联免疫吸附试验法显示通路抑制后,TNF-α、IL-1α、IL-6、IL-8和GM-CSF等炎症因子的分泌也明显降低.结论 TNF-α、IL-1α、IL-6、IL-8和GM-CSF等炎症因子可能通过NF-κB通路促进口腔鳞状细胞癌细胞转移.     

重组人β防御素3对牙龈卟啉单胞菌脂多糖致炎作用的影响

目的:以牙龈卟啉单胞菌脂多糖(P.g-LPS)诱发载脂蛋白E基因敲除(ApoE-/-)小鼠和RAW264.7小鼠单核巨噬细胞的急性炎症反应,并应用重组人β防御素3(rhBD3),观察其对炎症的干预效果。方法:20周龄雄性ApoE-/-小鼠随机均分为PBS对照组、P.g-LPS组和P.g-LPS+rhBD3组,分别经腹腔注射给药2h后,检测血清中不同炎症指标(MCP-1、TNF-α、IL-6、IL-1β和NO)的水平。同时,以rhBD3干预P.g-LPS对RAW264.7细胞的致炎作用,分别检测培养上清和细胞中炎症指标的水平及其mRNA的相对表达量。结果:经P.g-LPS刺激后,ApoE-/-小鼠血清MCP-1、TNF-α、IL-6和NO的水平较对照组显著上调;而同时应用rhBD3能明显降低MCP-1、TNF-α和NO表达量。P.g-LPS能显著上调RAW264.7细胞培养上清中TNF-α和NO的水平以及细胞中TNF-α和IL-6的mRNA相对表达量,rhBD3对此具有抑制作用。结论:rhBD3对P.g-LPS在体内、外诱导的急性炎症具有一定的抑制效应,可能在牙周炎与高脂血症的相互作用中发挥免疫调节作用。     

Aggregatibacter actinomycetemcomitans lipopolysaccharide stimulated epithelial cells produce interleukin-15 that regulates T cell activation

ObjectiveOral epithelial cells act not only as mechanical barriers but also as immunological barriers by producing various mediators such as cytokines. Since, in periodontal disease, limited information is available regarding the role of oral epithelial cell-derived cytokines on T cell activation, we investigated the responses of human T cells (Jurkat cell) to cytokines in KB cells (an oral epithelial cell line) that had been stimulated with Aggregatibacter actinomycetemcomitans lipopolysaccharide (LPS).DesignTo evaluate T cell activation in response to the culture supernatant of KB cells, we examined cell proliferation and interferon gamma (IFN-γ) production, which is closely related to periodontal disease, in Jurkat cells. Culture supernatant of LPS-stimulated KB cells enhanced cell proliferation and IFN-γ production in Jurkat cells. To determine the active component within the culture supernatant, the production of epithelial cell-derived cytokines, interleukin-12 (IL-12), IL-15 and IL-18, in LPS-stimulated KB cells was analysed.ResultsIL-15, but not IL-18, was significantly increased in the culture supernatant of LPS-stimulated KB cells. Moreover, additional anti-IL-15 neutralizing antibody abolished culture supernatant-induced IFN-γ expression in Jurkat cells.ConclusionThese results suggest that periodontal pathogens induce the production of IL-15 from epithelial cells, and leading the activation of T cells in periodontal lesions.     

内毒素耐受对共培养的中性粒细胞和单核细胞分泌TNF-α和IL-8的影响

目的 观察脂多糖（lipopolysaccharides,LPS）诱导的耐受对共培养的中性粒细胞和人单核细胞株THP-1细胞表达抗炎因子肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）和趋化因子白介素-8（Inter leukin-8, IL-8)水平的影响。 方法 采用1 μg/mL牙龈卟啉单胞菌（Porphyromonas gingivalis, P. gingivalis）LPS 或1 μg /mL大肠杆菌（Escherichia coli,E.coli）LPS分别刺激共培养的中性粒细胞和THP-1细胞24 h,洗脱后,再次刺激24 h,诱导细胞产生耐受。采用ELISA技术检测细胞条件培养液中 TNF-α 和 IL-8 表达水平的变化。 结果 P.gingivalis LPS或E.coli LPS单次刺激后,共培养的中性粒细胞和THP-1细胞分泌TNF-α和IL-8的水平均较刺激前明显增高（P＜0.05）;P.gingivalis LPS和E.coli LPS重复刺激后,共培养的中性粒细胞和THP-1细胞分泌的TNF-α水平较单次刺激后明显降低（P＜0.05）,但IL-8水平较单次刺激后明显增高（P＜0.05）。 结论 共培养的中性粒细胞和单核细胞产生的内毒素耐受可能抑制TNF-α表达,促进IL-8表达,进而可能影响牙周组织的炎症和免疫反应。     

肿瘤坏死因子α对体外培养人牙囊细胞血管内皮生长因子表达的影响

目的研究肿瘤坏死因子α(TNF-α)对体外培养人牙囊细胞血管内皮生长因子(VEGF)表达的影响。方法原代培养人牙囊细胞,传代至第4代,采用反转录聚合酶链反应(RT-PCR)及酶联免疫吸附试验(ELISA)分别检测TNF-α对体外培养人牙囊细胞VEGF mRNA表达及上清液中VEGF含量改变的浓度和时间效应。结果①不同浓度TNF-α作用1h后,TNF-α处理组人牙囊细胞VEGF mRNA表达均较对照组增强(P<0.05),最佳效应浓度为25ng/ml;不同浓度TNF-α作用12h后,除1ng/ml组外,其余各组上清液中VEGF蛋白含量明显高于对照组(P<0.05)。②在时间效应上,25ng/mlTNF-α作用1h后人牙囊细胞VEGF mRNA表达最强,然后随时间延长其表达逐渐下降,但仍强于对照组(P<0.05);细胞培养上清液中VEGF蛋白含量随时间延长逐渐增加,但TNF-α处理组VEGF蛋白含量高于对照组(P<0.05)。结论TNF-α能够促进体外培养人牙囊细胞合成并分泌VEGF。     

interleukin-1β and tumor necrosis factor-α stimulate synergistically the expression of monocyte chemoattractant protein-1 in fibroblastic cells derived from human periodontal ligament

The present study demonstrates that interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) induce and synergistically stimulate monocyte chemoattractant protein-1 (MCP-1) expression in fibroblasts from human periodontal ligament. IL-1β and TNF-α induced in a dose-dependent manner the expression of the MCP-1 gene in the fibroblasts from the human periodontal ligament. However, such an inducing effect was not observed with IL-6 and interferon-γ. The peak expression of the MCP-1 gene by IL-1β or TNF-α was observed at 3 h after initiation of their treatment. Furthermore, IL-1β in combination with TNF-α synergistically stimulated the MCP-1 gene expression in the cells. We also observed significant chemotactic activity for human monocytes in conditioned medium of fibroblasts from the human periodontal ligament treated with both cytokines. The stimulated chemotactic activity induced by these cytokines depended on both dose and treatment time. The chemotactic activity in conditioned medium of IL-1β-treated fibroblasts from the human periodontal ligament was neutralized by antiserum specific for MCP-1 protein. The MCP-1 gene product in conditioned medium of IL-1β-treated fibroblasts from the human periodontal ligament was shown to have a molecular mass of 11,000 Da by immunoprecipitation with the specific antiserum, and IL-1β also stimulated synergistically MCP-1 protein expression in combination with TNF-α. These results suggest that IL-1β and TNF-α may contribute to the infiltration of monocytes into inflammatory sites of periodontal ligament tissues via the MCP-1 gene product produced by fibroblasts from the human periodontal ligament.     

前列腺素E2、肿瘤坏死因子α、白细胞介素1β不同组合对培养骨器官钙代谢的作用

目的：观察不同浓度组合的前列腺素E2（PGE2）、肿瘤坏死因子α（TNF－2）、白细胞介素1β（IL－1β）对培养骨组织钙代谢的作用。方法：原子吸收分光光度计检测骨组织培养上清液中Ca^2 浓度。结果：①PGE2＋IL－1β：在0．01－1．0ng／ml浓度组合时，有促进钙吸收的作用，此作用随组合浓度的加大而减弱。②PGE2＋TNF－α：0．01－0．1ng／ml浓度时，有钙吸收作用，而在1．0ng／ml浓度组合时，有明显的钙释放作用。③IL－1β＋TNF－α：0．01ng／ml浓度组合时，有钙吸收作用。0．1ng／ml浓度组合时，钙吸收、释放作用不明显。1．0ng／ml浓度组合时，强刺激脱钙。④PGE2＋TNF－α＋IL－1β：0．01－1．0ng／ml浓度组合时显示钙吸收作用，且随剂量增加而增加。结论：3种细胞因子不同组合后，有交互作用、拮抗作用和协同作用。PGE2主要表现为协同因子而发挥作用。     

Correlations between pentraxin 3 or cytokine levels in gingival crevicular fluid and clinical parameters of chronic periodontitis

The gingival crevicular fluid (GCF) contains various biomarkers, such as interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α), and IL-10, among others. These cytokines have been reported to correlate with gingival inflammation and periodontal status. Therefore, the analysis of GCF may be useful for the diagnosis of periodontal status. Pentraxin 3 (PTX3) is the first identified long pentraxin, and is released by several cell types in response to proinflammatory signals. The aim of this study was to determine the levels of IL-1β, IL-6, IL-8, TNF-α, IL-10 and PTX3 in GCF from diseased and healthy sites in patients with chronic periodontitis. Cross-sectional clinical data were obtained from 50 patients with chronic periodontitis. GCF samples were collected with paper strips from one periodontal diseased site and one periodontally healthy site per subject. The levels of IL-1β, IL-6, IL-8, IL-10 and TNF-α were determined using a multiplexed bead immunoassay, and the PTX3 level was measured using an enzyme-linked immunosorbent assay. Mean clinical parameters were significantly higher at diseased sites (P < 0.01) as compared to healthy sites, and the mean levels of PTX3, IL-1β, IL-6, IL-8, IL-10 and TNF-α were higher in diseased sites (P < 0.01) than in healthy sites. There were strong correlations between PTX3 or IL-1β and periodontal status. These results suggest that GCF PTX3 levels might be useful as a diagnostic marker for periodontal disease.     

白藜芦醇减轻LPS诱导的牙周膜细胞损伤并抑制TLR4/NF-κB活化

目的:探究白藜芦醇(RES)对脂多糖(LPS)诱导的人牙周膜细胞(hPDLCs)损伤的保护作用.方法:体外培养并鉴定hPDLCs,将培养的hPDLCs随机分为5组:对照组、LPS(10 μg/ml)+RES(0、30、60、90tμmol/L)组,MTT法检测各组细胞增殖能力,ELISA检测各组细胞分泌TNF-α/IL-6水平,PCR和Western blot检测各组细胞TLR4/NF-κB mRNA和蛋白表达.结果:分离培养的hPDLCs抗波丝蛋白表达阳性,抗角蛋白表达阴性.与对照组比,LPS处理后细胞增殖能力明显降低,细胞分泌TNF-α/IL-6水平和TLR4/NF-κB mRNA和蛋白表达明显增加;30～90 μmol/L白藜芦醇预处理后,细胞增殖能力增加(P＜0.05),细胞分泌TNF-α/IL-6水平、TLR4/NF-κB mRNA以及蛋白表达则下调(P＜0.05),均呈现一定的浓度依赖性.结论:白藜芦醇可抑制TLR4/NF-κB活化并减轻LPS诱导的牙周膜细胞损伤.     

肿瘤坏死因子α对培养骨器官钙代谢的作用

目的：观察TNF－α对骨组织钙代谢的作用。方法：原子吸收分光光度计微量元素检测。结果：0．01－100ng/mlTNF－α的脱钙能力随着浓度的增加而减弱。结论：TNF－α的脱钙能力与其浓度呈负相关。     

Interleukin-1 alpha, interleukin-8 and interferon-alpha levels in gingival crevicular fluid

Cytokines play an important role in the pathology associated with chronic inflammatory diseases. We measured the total amounts [picograms (pg)] and concentrations (pg/μl) of interleukin-1 alpha (IL-lα), interleukin-8 (IL-8) and interferonalpha (IFN-α) in 20 s gingival crevicular fluid (GCF) samples obtained from 2 diseased and 2 healthy sites in 20 subjects with periodontitis, and from 2 healthy sites in 20 subjects without disease. Both the mean amount and concentration of IL-lα were significantly higher (p < 0.001) in diseased sites compared to healthy sites in subjects with disease. The results for IL-8 and IFN-α differed depending on the method of reporting. Whereas the amount of IL-8 was significantly higher (p < 0.01) in diseased sites, the mean concentration of IL-8 was lower compared to healthy sites. The mean amount of IFN-α was similar in health and disease; however, the concentration of IFN-alpha was significantly lower in diseased sites (p < 0.001) corresponding to the significant increase in crevicular fluid volume (p < 0.001). There were no significant differences in the amount or concentrations of the 3 cytokines between healthy sites from subjects with disease and healthy sites from healthy controls. The total amounts of both IFN-α and IL-8 were correlated between healthy and diseased sites in subjects. These data suggest that, while the disease status of a site is the major determinant of the levels of these cytokines locally, subjects with high levels of IL-8 and IFN-α in healthy sites also tend to have high levels of these cytokines in diseased sites. Finally, both the concentrations and total amounts of IL-8 and IFN-α were significantly correlated in diseased sites, suggesting that levels of these two cytokines rise or fall in tandem. The combination of decreased IL-8 and decreased IFN-α concentrations at diseased sites may reflect the reduced anti-bacterial host defense activity at that site.     

Cytokine levels in gingival crevicular fluid during orthodontic treatment with aligners compared to conventional labial fixed appliances: a 3-week clinical study

Objective: To test the hypothesis that the levels of IL-1ß and TNF-α increased more and IL-1α, IL-2, IL-6, IL-8 increased less, after 3 weeks of treatment with conventional labial fixed appliance and with aligners.

Material and methods: Forty patients who were treated either with labial brackets (n?=?20) or aligners (n?=?20). Gingival crevicular fluid (GCF) samples were collected at baseline and after 21 days. Cytokine levels were evaluated by enzyme-linked immune sorbent assay (ELISA). Plaque index (PI), gingival index (GI), and bleeding on probing (POB) were also examined.

Results: The levels of IL-1α, IL-1ß, IL-2, IL-6, IL-8 and TNF-α in the GCF were significantly increased in both groups. The levels of IL-2, IL-6, IL-8 increased more in patients treated with aligners compared to those treated by labial fixed appliances. There was a statistically significant difference in change of the mean cytokine levels of IL-1α, IL-2, IL-6, IL-8 and TNF-α compared to labial fixed appliances and aligners.

Conclusions: The levels of the six studied cytokines in GCF (IL-1α, IL-1ß, IL-2, IL-6, IL-8 and TNF-α) increased after 3 weeks both after treatment with conventional labial fixed appliance and with aligners. IL-1ß and TNF-α showed a prominent increase compared to the other cytokines in the GCF of teeth by both the labial fixed appliance and aligners. However, there were only minor differences in the changes of the cytokine levels from baseline to 3 weeks between the two groups. There were no differences between the groups regarding PI, GI or POB.     

Porphyromonas gingivalis induces myocarditis and/or myocardial infarction in mice and IL-17A is involved in pathogenesis of these diseases

ObjectivesAlthough an association between periodontitis and cardiovascular diseases has been suggested, the role of Porphyromonas gingivalis in cardiovascular diseases is not clear. In this study, we examined whether experimental bacteremia of P. gingivalis causes cardiovascular diseases and investigated the mechanism of pathogenesis of cardiovascular diseases induced by P. gingivalis.DesignC57BL/6 mice were intravenously inoculated with 2.0 × 10⁸ CFU of P. gingivalis A7436 strain. Mice were sacrificed at specified days and their hearts were collected. The collected organs were divided into two halves and used for histological evaluation and cytokine analysis. IL-17A^?/?, IFN-γ^?/? and TNF-α^?/? mice were also intravenously inoculated and the histological changes of hearts in mice were examined.ResultsMyocarditis and/or myocardial infarction were observed in mice injected with P. gingivalis. The levels of IL1-β, IL-6, IL-17A, IL-18, TNF-α and IFN-γ mRNA increased significantly after P. gingivalis injection. In particular, high levels of IL-17A and IFN-γ mRNA expression were observed in hearts of mice after P. gingivalis injection in comparison with these levels before injection. Furthermore, the production of IL-17A was detected in hearts of wild-type mice after P. gingivalis injection. In wild-type, TNF-α^?/? and IFN-γ^?/? mice, moderate infiltration of neutrophils and monocytes was observed in hearts at 5 days after injection. In contrast, no inflammatory findings were observed in hearts of IL-17A^?/? mice.ConclusionWe have demonstrated that an experimental bacteremia of P. gingivalis could induce myocarditis and/or myocardial infarction in mice, and IL-17A plays an important role in the pathogenesis of these diseases.     

Hinokitiol increases the angiogenic potential of dental pulp cells through ERK and p38MAPK activation and hypoxia-inducible factor-1α (HIF-1α) upregulation

Hinokitiol, a natural iron-chelating agent, is known to have diverse biological and pharmacological activities in various cell types. However, the effect of hinokitiol on dental pulp cells has not yet been reported. In this study, hinokitiol increases hypoxia-inducible factor-1α (HIF-1α) protein levels and vascular endothelial growth factor (VEGF) secretion in human dental pulp cells. The extracellular-signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) pathways are involved in hinokitiol-induced HIF-1α protein expression in dental pulp cells. Conditioned media from hinokitiol-treated pulp cells enhances angiogenesis in vitro and in vivo. Overall, these results show that hinokitiol promotes ERK and p38MAPK activation and HIF-1α-induced VEGF production, thus increasing the angiogenic potential of dental pulp cells.     

Increased tumor-infiltrating plasmacytoid dendritic cells predicts poor prognosis in oral squamous cell carcinoma

ObjectiveAccumulating evidence suggests that plasmacytoid dendritic cells (pDC) have a dual role not only in initiating anti-tumor immune responses but also in inducing immune tolerance to facilitate cancer development. The aim of this study was to investigate the distribution and function of tumor-infiltrating pDCs in primary oral squamous cell carcinoma (OSCC) and their relation to patient outcome.MethodsThe distribution of pDCs in 10 normal oral mucosa and 60 OSCC tissues was detected by immunohistochemistry. The population of pDCs in six OSCC patients and six healthy donors was evaluated by flow cytometry. The relationship between tumor-infiltrating pDCs and clinicopathological data and patient outcome was analyzed accordingly. The capacity of pDCs to produce cytokines, such as IFN-α, IL-6, IL-8 and TNF-α in response to TLR-9 ligands (CpG-ODN) was measured by ELISA.ResultPDCs were detected at high levels in 38.3% of the OSCC tissues, primarily in the stroma, but were absent in normal oral mucosa. The frequency of pDCs in OSCC tissue was significantly higher than that observed in normal oral mucosa. However, the distribution and population of circulating pDCs was similar between healthy donors and OSCC patients. Kaplan-Meier analysis revealed a significant association of increasing number of tumor-infiltrating pDCs with lymph node metastasis and overall survival. Multivariate analysis confirmed that high levels of tumor-infiltrating pDCs was an independent prognostic factor. Further cytokine analysis revealed a decreased secretion of IFN-α, IL-6 and TNF-α, which indicated an impaired function of tumor-infiltrating pDCs.ConclusionsThe increased number of tumor-infiltrating pDCs correlates with an adverse outcome in primary OSCC patients. This finding is not only suggestive of the contribution of pDCs in the progression of oral cancer but also presents an opportunity and a new target for OSCC immune therapy in oral cancer management.     

血清白细胞介素20在牙周炎及慢性阻塞性肺疾病中作用的初步探讨

目的初步探讨血清白细胞介素20（IL-20）及白细胞介素6（IL-6）、肿瘤坏死因子（TNF-α）在牙周炎及慢性阻塞性肺疾病（COPD）中的作用。方法选取151例患者,按牙周炎及COPD的严重程度分为四组,采用酶联免疫吸附法（ELISA）测定四组患者血清中IL-20、IL-6和TNF-α的浓度。结果中重度牙周炎伴COPD患者血清中IL-20、IL-6和TNF-α的水平显著高于对照人群,并且两种疾病并存时,血清IL-20水平较单独存在时高。结论血清中IL-20及IL-6、TNF-α水平的高表达可能与牙周炎及COPD的发病机理有关,加重两种疾病炎症反应过程。     

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目的评价贵金属烤瓷全冠修复体对患牙牙周组织的影响。方法选择2007年4月至2008年12月于沈阳市沈河区牙病防治所行贵金属烤瓷全冠修复的患者25例(患牙77颗),于修复前和修复后6、12个月分别进行常规龈沟出血指数(SBI)检查、龈沟液(GCF)称量及GCF中白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)检测。结果肩台设计为龈下的前牙SBI在修复后12个月与修复前比较差异有统计学意义(P<0.05),GCF质量及GCF中IL-1β和TNF-α含量在修复前与修复后6个月、12个月比较差异无统计学意义(P>0.05);肩台设计为龈上的磨牙SBI、GCF质量及GCF中IL-1β和TNF-α含量在修复前与修复后6个月、12个月比较差异无统计学意义(P>0.05)。结论贵金属烤瓷全冠修复体对患牙的牙周组织影响较小,有利于牙周健康。     

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目的探讨钴铬合金烤瓷全冠修复对患牙牙周组织的影响。方法选择2007年4月至2008年10月来沈阳市沈河区牙病防治所应用钴铬合金烤瓷全冠修复的患者39例(106颗患牙),修复前和修复后6、12个月分别进行常规龈沟出血指数(SBI)检查,龈沟液(GCF)称量,GCF中白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)质量浓度的检测。结果修复前牙的患者患牙SBI、GCF质量、GCF中IL-1β和TNF-α的质量浓度修复前与修复后6个月比较差异无统计学意义(P>0.05),与修复后12个月比较差异有统计学意义(P<0.05);修复后牙的患者患牙SBI、GCF质量修复前与修复后6个月比较差异无统计学意义(P>0.05),与修复后12个月比较差异有统计学意义(P<0.05);修复后牙的患者患牙GCF中IL-1β和TNF-α的质量浓度修复前与修复后6个月和修复后12个月比较差异均无统计学意义(P>0.05)。结论采用钴铬合金烤瓷全冠修复前牙,修复时间超过12个月时,对SBI、GCF质量和GCF中IL-1β和TNF-α的质量浓度有显著影响;修复后牙,修复时间超过12个月时,对SBI、GCF质量有显著影响,而对GCF中IL-1β和TNF-α的质量浓度无明显影响。     

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目的 探讨双氯芬酸钠对脂多糖（LPS）诱导的人牙周膜成纤维细胞（HPDLFs）白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）表达的影响。方法 本研究于2013年3—5月在山西医科大学口腔实验室进行。将复苏培养冻存的HPDLFs进行形态学鉴别后,用10 μg/mL的LPS进行诱导,分别以0.1、1、10、50、100 mg/L的双氯芬酸钠进行干预,酶联免疫吸附试验法（ELISA法）检测HPDLFs表达IL-1β和TNF-α水平的变化。结果 对同一质量浓度LPS诱导的HPDLFs而言,双氯芬酸钠能下调HPDLFs表达IL-1β和TNF-α的水平,并且随着双氯芬酸钠质量浓度的增加,IL-1β和TNF-α的表达量呈逐渐减弱的趋势（P＜0.05）。结论 双氯芬酸钠可能对于LPS诱导的HPDLFs IL-1β和TNF-α的表达有重要的抑制作用,这为牙周病的临床治疗提供了新的思路。