首页> 外文期刊>Journal of Endodontics: Official Journal of American Association of Endodontists >The survival role of peroxisome proliferator-activated receptor gamma induces odontoblast differentiation against oxidative stress in human dental pulp cells
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The survival role of peroxisome proliferator-activated receptor gamma induces odontoblast differentiation against oxidative stress in human dental pulp cells

机译:过氧化物酶体增殖物激活受体γ的生存作用诱导成牙本质细胞分化为人类牙髓细胞中的氧化应激

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Introduction: Peroxisome proliferator-activated receptor gamma (PPAR??) has well-known anti-inflammatory action in human dental pulp cells (HDPCs). The purpose of this study was to investigate whether the anti-inflammatory action of PPAR?? involves in cellular cytoprotection and supports odontoblast differentiation under oxidative stress in HDPCs. Methods: To simulate long-term oxidative stress, pulp cells were treated with 150 ??mol hydrogen peroxide (H2O2) for 12 days. The replication deficiency adenovirus (adenovirus PPAR??) was introduced for PPAR?? overexpression in pulp cells. The cellular cytotoxicity and reactive oxygen species formation by H2O2 were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and 2??,7??-dichlorodihydrofluorescein diacetate with fluorescence- activated cell sorting assay. To determine the roles of PPAR??, several molecules of odontogenic/osteogenic and signal pathway were analyzed by reverse-transcription polymerase chain reaction and Western hybridization. Dentin mineralization was determined by alizarin red stain and alkaline phosphatase activity assay. Results: Pulp cells treated with long-term H 2O2 showed high reactive oxygen species formation, low cell viability, down-expression of antioxidant molecules (Cu/Zn and Mn superoxide dismutase), and odontogenic/osteogenic markers (eg, dentin sialophosphoprotein, dentin matrix protein-1, osteopontin, bone sialoprotein, Runx-2, and bone morphogenetic protein 2 and 7). In addition, pulp cells with oxidative stress underwent the activation of ERK1/2, activator protein-1, and nuclear factor-??B translocation to the nucleus. However, the PPAR??-overexpressed cells gave opposite results although under oxidative stress. Furthermore, PPAR?? and its agonist rosiglitazone exhibited an induction of dentin mineralization under oxidative stress. Conclusions: PPAR?? in pulp cells increases cell viability, odontoblastic differentiation, and dentin mineralization under oxidative stress. These results offer new insights into the potential antioxidative activity of PPAR?? and its agonist for therapeutic agents for pulp vitality in HDPCs.
机译:简介:过氧化物酶体增殖物激活受体γ(PPARα)在人牙髓细胞(HDPC)中具有众所周知的抗炎作用。这项研究的目的是调查PPAR的抗炎作用。 HDPC参与细胞的细胞保护并支持成牙本质细胞在氧化应激下的分化。方法:为了模拟长期的氧化应激,用150 mol的过氧化氢(H2O2)处理果肉细胞12天。为PPARα3引入了复制缺陷型腺病毒(腺病毒PPARα2)。牙髓细胞过度表达。通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物和2,7,7′-二氯二氢荧光素二乙酸酯,通过荧光激活细胞分选法测定H2O2对细胞的细胞毒性和活性氧的形成。分析。为了确定PPARα的作用,通过逆转录聚合酶链反应和Western杂交分析了几种成牙/成骨分子和信号途径。通过茜素红染色和碱性磷酸酶活性测定法测定牙本质矿化。结果:经长期H 2 O 2处理的纸浆细胞表现出高活性氧形成,低细胞活力,抗氧化剂分子(Cu / Zn和Mn超氧化物歧化酶)表达降低以及成牙/成骨标志物(例如牙本质唾液磷蛋白,牙本质)基质蛋白1,骨桥蛋白,骨唾液蛋白,Runx-2以及骨形态发生蛋白2和7)。另外,具有氧化应激的牙髓细胞经历了ERK1 / 2,活化蛋白-1和核因子-βB向细胞核的转移。然而,尽管在氧化应激下,PPARα-过表达的细胞给出相反的结果。此外,PPAR ??其激动剂罗格列酮在氧化应激下具有诱导牙本质矿化的作用。结论:PPAR?果肉细胞中的α-淀粉样蛋白可增加细胞活力,成牙本质细胞分化和氧化应激下的牙本质矿化。这些结果提供了对PPAR潜在抗氧化活性的新见解。及其作为HDPC纸浆活力治疗剂的激动剂。

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