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作 者:闫艳梅[1,2] 唐亚平[1] 贺涛 马灿灿 方慧[1] 钟雯怡[1] 刘琪[1]
机构地区:[1]遵义医学院附属口腔医院,贵州遵义563003 [2]岳阳市一人民医院口腔科,湖南岳阳414000 [3]长沙市口腔医院,湖南长沙410005 [4]邹城市口腔医院,山东邹城273500
出 处:《口腔医学研究》2017年第3期269-272,共4页Journal of Oral Science Research
基 金:国家自然基金(编号:81360168);贵州省科学技术基金;黔科合字(2014)7596号;遵义市科技支撑计划项目;遵市科合社字(2013)31号
摘 要:目的:探讨1,25(OH)2D3对2型糖尿病伴牙周炎患者中性粒细胞(Polymorphonuclear leukocytes,PMN)凋亡及炎性介质表达的影响。方法:采用密度梯度离心法分离2型糖尿病伴牙周炎患者外周血PMN,然后于含或不含1,25(OH)2D3培养液中培养24h,分别运用流式细胞术(FCM)检测PMN凋亡率;酶联免疫吸附试验(ELISA)检测上清液中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、中性粒细胞弹性蛋白酶(neutrophil elastase,NE)的含量变化。结果:与1,25(OH)2D3未干预组相比,1,25(OH)2D3干预组PMN凋亡率均升高,P<0.05;1,25(OH)2D3干预组两两比较发现,10-8 mol/L干预组PMN凋亡率>10-6mol/L干预组>10-10 mol/L干预组(P<0.05)。ELISA检测PMN上清液中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、中性粒细胞弹性蛋白酶(NE)的结果显示,1,25(OH)2D3干预组TNF-α、IL-1β、IL-6、NE的水平均较未干预组低(P<0.05)。结论:1,25(OH)2D3能够促进PMN凋亡,下调炎性介质的表达,在2型糖尿病伴牙周炎的发生、发展中可能起免疫调节作用。Objective:To investigate the effect of 1,25(OH)2D3on neutrophils apoptosis and inflammatory mediators expression in Type 2diabetic patients with chronic periodontitis.Methods:Neutrophils were isolated by density gradient centrifugation from Type 2diabetic patients with chronic periodontitis peripheral blood and cultured in media with or without 1,25(OH)2D3for 24 h.The apoptosis rate of neutrophils was detected by flow cytometry(FCM).Expressions of tumor necrosis factor-α,interleukin-1β,interleukin-6,and neutrophil elastase in supernatants were tested by enzyme-linked immunosorbent assay(ELISA).Results:Flow cytometry analysis showed that 1,25(OH)2D3intervention group neutrophil apoptosis rate was increased significantly(P〈0.05).Multiple comparison revealed that there were significant differences among groups with different concentrations(10-8 mol/L intervention group10-6 mol/L intervention group10-10 mol/L intervention group).ELISA results showed that tumor necrosis factor-α,interleukin-1β,and interleukin-6content were decreased in 1,25(OH)2D3intervention group(P〈0.05).Conclusion:1,25(OH)2D3 may promote the neutrophil apoptosis and decrease the expression of inflammatory mediators,and play an immune regulatory role in the occurrence and development in Type 2diabetic patients with chronic periodontitis.
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