J Endod:细菌感染时人牙髓细胞表达炎症及硬组织形成相关细胞标志物

2018-05-03 lishiting MedSci原创

脂多糖(LPS)是引起深龋和牙髓炎时革兰阴性菌外膜的主要组成部分。当细菌侵入牙本质小管和牙本质持续受到损伤时,预先存在的成牙本质细胞会形成修复性牙本质。然而,LPS与修复性牙本质的关系还未可知。这篇研究的目的是为了评估LPS刺激是否会诱导人牙髓细胞(hDPCs)的硬组织形成。

脂多糖(LPS)是引起深龋和牙髓炎时革兰阴性菌外膜的主要组成部分。当细菌侵入牙本质小管和牙本质持续受到损伤时,预先存在的成牙本质细胞会形成修复性牙本质。然而,LPS与修复性牙本质的关系还未可知。这篇研究的目的是为了评估LPS刺激是否会诱导人牙髓细胞(hDPCs)的硬组织形成。研究培养永生化的dDPCs,将埃希氏菌来源的LPS (1 μg/mL)加入培养基中。在培养0, 1, 3, 7, 14和21天后获取样本,检测IL-1β, IL-6, Wnt5a, Runx2, ALP的信使RNA表达情况,并检测ALP活性。定量PCR结果显示,LPS组在刺激1天时IL-1β和IL-6的表达显著升高(P < .05)。14天时,LPS组的Wnt5a, Runx2和ALP的表达明显高于对照组(分别为2.0-, 4.7-和10.0-fold) (P < .01)。21天时,LPS组的ALP活性显著高于对照组(P < .01)。施加Wnt5a的抑制剂Box5,会减弱Runx2和ALP的表达(P < .05)。结论:这些结果表明,LPS刺激可以通过Wnt5a信号通路诱导hDPCs炎症

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    2018-12-08 mnda
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    2018-09-13 jxrzshh
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    2018-05-05 chengjn

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