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作 者:吕晶露 卞添颖 李丽丽[1] 崔迪[1] 张婷[1] 雷浪[1] 闫福华[1]
机构地区:[1]南京大学医学院附属口腔医院牙周科,江苏南京210008
出 处:《口腔医学研究》2015年第12期1179-1183,共5页Journal of Oral Science Research
基 金:国家自然科学基金项目(编号:81371152);江苏省自然科学基金项目(编号:BK20131079);江苏省临床科技专项(编号:BL2013002)
摘 要: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。Objective:To investigate the effects of recombinant human beta-defensin-3(rhBD3)on acute inflammation induced by Porphyromanas gingivilis lipopolysaccharide(P.g-LPS)in apolipoprotein E knockout(ApoE-/-)mice and murine RAW264.7macrophages.Methods:Male ApoE-/- mice(20weeks old)were randomly divided into PBS control group,P.g-LPS group and P.g-LPS+rhBD3group,and were stimulated by intraperitoneal injection.Serum inflammation markers(MCP-1,TNF-α,IL-6,IL-1βand NO)secretion levels were measured 2hours later.The effects of rhBD3 on inflammation induced by P.g-LPS in RAW264.7cells were also evaluated by detecting the secretion levels and mRNA relative expression levels of inflammation markers in culture supernatant and cells,respectively.Results:Serum MCP-1,TNF-α,IL-6and NO secretion levels in P.g-LPS group of ApoE-/- mice were significantly upregulated,while the levels of MCP-1,TNF-αand NO decreased significantly in P.g-LPS+rhBD3group.The increased levels of TNF-αand NO in culture supernatant and mRNA relative expression levels of TNF-αand IL-6in RWA264.7cells stimulated by P.g-LPS could be downregulated by rhBD3.Conclusion:rhBD3has suppressive effect on acute inflammation induced by P.g-LPS in vivo and in vitro.It may play a modulating role in the interaction between periodontitis and hyperlipidemia.
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