AIM To characterize a lipopolysaccharide (LPS)-treated dentine tissue model (LPS dentine) to analyse the efficacy of polycationic chitosan nanoparticles (CSnp) and/or dexamethasone conjugate chitosan nanoparticles (Dex-CSnp) on the viability/differentiation potential of stem cells from apical papilla (SCAP) when exposed to LPS dentine. A further aim was to understand the effect of macrophage-dependent inflammation on SCAP migration in the presence of LPS dentine. METHODOLOGY A total of 88 dentine slabs were used. TOF-SIMS analysis was performed amongst the LPS-treated and untreated dentine groups (n = 2/group). The study was conducted using four dentine groups: no treatment (control); LPS treatment only; LPS treatment followed by CSnp conditioning; and LPS treatment followed by Dex-CSnp conditioning groups. SCAP adherence, viability, differentiation and biomineralization potential on dentine from different groups were studied using fluorescent and scanning electron microscopy. Inflammation by macrophages in response to LPS dentine was quantified, and effect on SCAP migration was analysed. Statistical analysis was performed using Student's t-test with a significance level of P < 0.05. RESULT TOF-SIMS analysis confirmed LPS contamination. LPS dentine affected SCAP viability but not adherence to dentine (P < 0.001). Conditioning of LPS dentine with either nanoparticles improved SCAP viability (P < 0.01) and rescued other LPS related adverse effects on SCAPs, such as F-actin disruption, decrease in differentiation/biomineralization potential. IL-6 produced by macrophages in response to LPS-treated dentine impeded SCAP migration (P < 0.001), diminished on CSnp and Dex-CSnp conditioning groups (P < 0.01). CONCLUSION This study developed an LPS-dentine model and highlighted the ability of CSnp and Dex-CSnp to promote stem cell viability, migration, differentiation potential and reduce inflammation, providing an environment conducive for tissue regeneration/repair.

中文翻译：

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生物活性纳米粒子对组织内毒素的诱导诱导的干细胞活力，迁移和分化的抑制作用。

目的表征经脂多糖（LPS）处理的牙本质组织模型（LPS牙本质），以分析聚阳离子壳聚糖纳米颗粒（CSnp）和/或地塞米松共轭壳聚糖纳米颗粒（Dex-CSnp）对来自干细胞的活力/分化潜能的功效暴露于LPS牙本质时为根尖乳头（SCAP）。另一个目的是了解在LPS牙本质存在下巨噬细胞依赖性炎症对SCAP迁移的影响。方法总共使用了88个牙本质板。在LPS治疗和未治疗的牙本质组（n = 2 /组）之间进行TOF-SIMS分析。该研究使用四个牙本质组进行：未治疗（对照）；未治疗 仅LPS治疗；LPS处理，然后进行CSnp调节；和LPS治疗，然后进行Dex-CSnp调理组。遵守SCAP，生存能力，使用荧光和扫描电子显微镜研究了不同组牙本质的分化和生物矿化潜力。定量了巨噬细胞对LPS牙本质的炎症反应，并分析了其对SCAP迁移的影响。使用Student's t检验进行统计学分析，显着性水平为P <0.05。结果TOF-SIMS分析确认了LPS污染。LPS牙本质影响SCAP的生存能力，但不影响牙本质的粘附性（P <0.001）。用任一纳米颗粒对LPS牙本质进行调理可提高SCAP活力（P <0.01），并挽救了其他与LPS相关的对SCAP的不利影响，例如F-肌动蛋白破坏，分化/生物矿化潜力降低。巨噬细胞对LPS处理的牙本质产生的IL-6阻碍了SCAP迁移（P <0.001），在CSnp和Dex-CSnp调节组上降低（P <0.01）。结论本研究建立了LPS-牙本质模型，并强调了CSnp和Dex-CSnp促进干细胞活力，迁移，分化潜能并减少炎症的能力，为组织再生/修复提供了有利的环境。