Betamethasone suppresses the inflammatory response in LPS-stimulated dental pulp cells through inhibition of NF-κB
Betamethasone suppresses the inflammatory response in LPS-stimulated dental pulp cells through inhibition of NF-κB
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Betamethasone 通过抑制 NF-κB 抑制 LPS 刺激的 T 牙髓细胞的炎症反应
DOI：
10.1016/j.archoralbio.2018.11.022
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发表时间：
2019-02-01
影响因子：
3
通讯作者：
Wang, Yuan-Yuan
中科院分区：
文献类型：
--
作者：
Wang, Dan;Zhu, Ning-Xin;Wang, Yuan-Yuan
目的：本研究旨在探讨betteramine对LPS刺激的人牙髓干细胞（DPSCs）的抗炎作用及其机制。评价倍他米松对DPSC和人脱落乳牙（SHED）干细胞的成骨/牙源性分化和破骨细胞作用。设计：使用八肽胆囊收缩素测定分析倍他米松对DPSC的增殖作用。采用定量聚合酶链反应（qPCR）和ELISA法研究倍他米松的抗炎作用。采用qPCR、Western blot、免疫荧光染色等方法探讨其抗炎机制。结果：1 μ g L-1 betterin对DPSCs增殖的作用最强，而10 μ g L-1 betterin对DPSCs增殖的作用最弱，10 μ g L-1 betterin对DPSCs增殖的作用最强。在LPS刺激的DPSC中，用倍他米松处理后，促炎细胞因子和介质以及前列腺素E-2（PGE（2））的表达显著降低。它们也因NF-κ B抑制剂Bay 11-7082而减少。倍他米松和Bay 11-7082显着抑制p-p65的表达并促进p65的核排斥。在betterone和成骨培养基（OM）处理组中，与成骨/牙向分化相关的基因表达显著上调。结论：betalone通过阻断NF-κ B的活化，对LPS刺激的DPSCs具有抗炎作用，并对DPSCs和SHED具有成骨/成牙诱导作用。虽然beta2对SHED显示破骨细胞作用。
Objective: This study aimed to investigate the anti-inflammatory effect of betamethasone on LPS-stimulated human dental pulp stem cells (DPSCs) and its associated mechanism. The osteo-/odontogenic differentiation and osteoclast effect of betamethasone on DPSCs and stem cells from human exfoliated deciduous teeth (SHED) were evaluated.Design: The proliferative effect of betamethasone on DPSCs was analyzed using a cholecystokinin octapeptide assay. The anti-inflammatory effect of betamethasone was investigated using quantitative polymerase chain reaction (qPCR) and ELISA. The anti-inflammatory mechanism was explored using qPCR, Western blot, and immunofitiorescence staining. The osteo-/odontogenic differentiation and osteoclast effect of betamethasone on DPSCs and SHED were detected by qPCR.Results: 1 mu g L-1 betamethasone was found to have the strongest effect on DPSCs proliferation. The expression of pro-inflammatory cytokines and mediators, as well as prostaglandin E-2 (PGE(2)) were significantly decreased following treatment with betamethasone in LPS-stimulated DPSCs. They were also decreased in response to an NF-kappa B inhibitor, Bay 11-7082. Betamethasone and Bay 11-7082 significantly inhibited the expression of p-p65 and promoted the nuclear exclusion of p65. Gene expression associated with osteo-/odontogenic differentiation was significantly up-regulated in betamethasone and osteogenic media (OM) treated groups. The ratio of the receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) at the mRNA level was suppressed in DPSCs and elevated in SHED.Conclusions: Betamethasone has an anti-inflammatory effect on LPS-stimulated DPSCs through a blockade of NF-kappa B activation and exhibits an osteo-/odonto-inductive effect an DPSCs and SHED. Although betamethasone displays an osteoclast effect on SHED.