Go6983 attenuates titanium particle-induced osteolysis and RANKL mediated osteoclastogenesis through the suppression of NFκB/JNK/p38 pathways
Go6983 attenuates titanium particle-induced osteolysis and RANKL mediated osteoclastogenesis through the suppression of NFκB/JNK/p38 pathways
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Go6983 通过抑制 NFkappaB/JNK/p38 途径减弱钛颗粒诱导的骨溶解和 RANKL 介导的破骨细胞生成
DOI：
10.1016/j.bbrc.2018.05.177
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发表时间：
2018-09-03
影响因子：
3.1
通讯作者：
Liu, Yun
中科院分区：
文献类型：
--
作者：
Feng, Wenyu;Li, Jia;Liu, Yun
磨损颗粒激活破骨细胞给外科医生带来了很大的困难。磨损颗粒是无菌假体松动的主要原因。Go6983是一种蛋白激酶C抑制剂，可抑制蛋白激酶C家族成员的五种亚型。在体内，我们发现Go6983对磨损颗粒诱导的骨溶解有明显的抑制作用。在体外，Go6983通过抑制rankl刺激的核因子κ B/JNK/p38信号通路抑制rankl刺激的破骨细胞形成和功能。我们还观察到Go6983对成骨细胞的分化和成骨细胞相关基因的表达没有影响。根据我们的数据，Go6983对破骨细胞活化引起的无菌性假体松动具有潜在的治疗作用。(C) 2018爱思唯尔公司版权所有。
Osteoclast activation by wear particles has caused major difficulties for surgeons. Wear particles are the main causes of aseptic prosthetic loosening. Go6983, a protein kinase C inhibitor, inhibits five subtypes of protein kinase C family members. Here, we found that Go6983 had an obviously inhibitory effect on wear-particles-induced osteolysis in vivo. In vitro, Go6983 inhibited RANKL-stimulated osteoclast formation and function by inhibiting the RANKL-stimulated nuclear factor-kappa B/JNK/p38 signaling pathway. We also observed that Go6983 had no effect on the differentiation of osteoblasts and osteoblast-associated genes expression. According to our data, Go6983 has potential therapeutic effects for aseptic prosthetic loosening caused by osteoclast activation. (C) 2018 Elsevier Inc. All rights reserved.