Objective:To study the effect of smoking on EA and NOS expression as well as NO and ET-1 content in gingival tissue of patients with chronic periodontitis.Methods: Patients diagnosed with periodontitis in our hospital...Objective:To study the effect of smoking on EA and NOS expression as well as NO and ET-1 content in gingival tissue of patients with chronic periodontitis.Methods: Patients diagnosed with periodontitis in our hospital between May 2013 and March 2016 were selected to screen 72 cases of smokers and 80 cases of non-smokers who were enrolled in smoking group and non-smoking group respectively, periodontal tissue was collected to detect the expression of EA, NOS and NLRP3 inflammasome, and gingival crevicular fluid was collected to detect the content of ET-1, NO, inflammatory factors and MMPs.Results:EA expression and ET-1 content in gingival tissue of smoking group were significantly higher than those of non-smoking group while NOS expression and NO content in gingival tissue were significantly lower than those of non-smoking group;NLRP3, ASC, Caspase-1, IL-1β and IL-18 expression in gingival tissue of smoking group were significantly higher than those of non-smoking group, and IL-1β, IL-18, TNF-α, IFN-γ, MMP1, MMP8 and MMP13 content in gingival crevicular fluid were significantly higher than those of non-smoking group;NLRP3, ASC, Caspase-1, IL-1β and IL-18 expression as well as IL-1β, IL-18, TNF-α, IFN-γ, MMP1, MMP8 and MMP13 content were positively correlated with EA and ET-1, and negatively correlated with NOS and NO.Conclusion:Smoking can cause increased EA and ET-1 as well as decreased NOS and NO in gingival tissue of patients with chronic periodontitis, thus adjusting the expression of NLRP3 inflammasome and MMPs to periodontal tissue inflammation and structure damage.展开更多
Inflammation and endothelial dysfunction are linked to the pathogenesis of atherosclerotic disease. Recent studies suggest that periodontal infection and the ensuing increase in the levels of inflammatory markers may ...Inflammation and endothelial dysfunction are linked to the pathogenesis of atherosclerotic disease. Recent studies suggest that periodontal infection and the ensuing increase in the levels of inflammatory markers may be associated with myocardial infarction, peripheral vascular disease and cerebrovascular disease. The present article aimed at reviewing contemporary data on the pathophysiology of vascular endothelium and its association with periodontitis in the scenario of cardiovascular disease.展开更多
目的:探讨鸢尾素调节Janus蛋白酪氨酸激酶2(Janus protein tyrosine kinase 2,JAK2)/信号转导和转录激活子3(Signal transduction and activator of transcription 3,STAT3)信号通路对牙周炎大鼠牙周组织损伤的影响。方法:通过结扎和接...目的:探讨鸢尾素调节Janus蛋白酪氨酸激酶2(Janus protein tyrosine kinase 2,JAK2)/信号转导和转录激活子3(Signal transduction and activator of transcription 3,STAT3)信号通路对牙周炎大鼠牙周组织损伤的影响。方法:通过结扎和接种牙龈卟啉单胞菌液建立牙周炎大鼠模型,将大鼠随机分为模型组、鸢尾素低(鸢尾素-L,50 mg/kg)、中(鸢尾素-M,100 mg/kg)、高剂量(鸢尾素-H,200 mg/kg)组、鸢尾素-H+激活剂(200 mg/kg鸢尾素+2 mg/kg香豆霉素)组,每组10只,并以注射等体积生理盐水的正常大鼠对照组。干预结束后,对大鼠牙龈出血指数、牙齿松动度评分;牙槽骨吸收、肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、白细胞介素(Interleukin,IL)-6、IL-1β以及丙二醛(Malondialdehyde,MDA)、超氧化物歧化酶(Superoxide dismutase,SOD)水平分别以Micro-CT试剂盒检测;HE检测牙周组织病理学变化;Western blot检测JAK2、STAT3、p-JAK2、p-STAT3蛋白表达。结果:与对照组相比,模型组大鼠牙周组织被破坏,炎性浸润严重,牙龈出血指数、牙齿松动度评分、牙槽骨吸收、TNF-α、IL-6、IL-1β、MDA水平、p-JAK2/JAK2、p-STAT3/STAT3表达显著增加,SOD水平显著降低(P<0.05);与模型组相比,不同剂量的鸢尾素组大鼠病理损伤得到改善,牙龈出血指数、牙齿松动度评分、牙槽骨吸收、TNF-α、IL-6、IL-1β、MDA水平、p-JAK2/JAK2、p-STAT3/STAT3表达显著降低,SOD水平显著增加,具有剂量依赖性(P<0.05);与鸢尾素-H组相比,鸢尾素-H组+激活剂组大鼠病理损伤加重,大鼠牙龈出血指数、牙齿松动度评分、牙槽骨吸收、TNF-α、IL-6、IL-1β、MDA水平、p-JAK2/JAK2、p-STAT3/STAT3表达显著增加,SOD水平显著降低(P<0.05)。结论:鸢尾素抑制牙周炎大鼠氧化应激、炎性反应,减轻大鼠牙周组织损伤,减少牙槽骨吸收,可能与抑制JAK2/STAT3信号通路有关。展开更多
文摘Objective:To study the effect of smoking on EA and NOS expression as well as NO and ET-1 content in gingival tissue of patients with chronic periodontitis.Methods: Patients diagnosed with periodontitis in our hospital between May 2013 and March 2016 were selected to screen 72 cases of smokers and 80 cases of non-smokers who were enrolled in smoking group and non-smoking group respectively, periodontal tissue was collected to detect the expression of EA, NOS and NLRP3 inflammasome, and gingival crevicular fluid was collected to detect the content of ET-1, NO, inflammatory factors and MMPs.Results:EA expression and ET-1 content in gingival tissue of smoking group were significantly higher than those of non-smoking group while NOS expression and NO content in gingival tissue were significantly lower than those of non-smoking group;NLRP3, ASC, Caspase-1, IL-1β and IL-18 expression in gingival tissue of smoking group were significantly higher than those of non-smoking group, and IL-1β, IL-18, TNF-α, IFN-γ, MMP1, MMP8 and MMP13 content in gingival crevicular fluid were significantly higher than those of non-smoking group;NLRP3, ASC, Caspase-1, IL-1β and IL-18 expression as well as IL-1β, IL-18, TNF-α, IFN-γ, MMP1, MMP8 and MMP13 content were positively correlated with EA and ET-1, and negatively correlated with NOS and NO.Conclusion:Smoking can cause increased EA and ET-1 as well as decreased NOS and NO in gingival tissue of patients with chronic periodontitis, thus adjusting the expression of NLRP3 inflammasome and MMPs to periodontal tissue inflammation and structure damage.
基金Supported by The Fundo de Incentivo à Pesquisa e Eventos(FIPE)at Hospital de Clínicas de Porto Alegre,No.HCPA-120265
文摘Inflammation and endothelial dysfunction are linked to the pathogenesis of atherosclerotic disease. Recent studies suggest that periodontal infection and the ensuing increase in the levels of inflammatory markers may be associated with myocardial infarction, peripheral vascular disease and cerebrovascular disease. The present article aimed at reviewing contemporary data on the pathophysiology of vascular endothelium and its association with periodontitis in the scenario of cardiovascular disease.
