作者: Fangfang Song , Hualing Sun , Yake Wang , Hongye Yang , Liyuan Huang
DOI: 10.1111/JCMM.12988
关键词: Pulpitis 、 MG132 、 Interleukin 、 NF-κB 、 NFKB1 、 Inflammation 、 Cancer research 、 Proteasome inhibitor 、 Immunology 、 Tumor necrosis factor alpha 、 Chemistry
摘要: Human dental pulp cells (HDPCs) play a crucial role in inflammation. Pannexin 3 (Panx3), member of Panxs (Pannexins), has been recently found to be involved However, the mechanism Panx3 human inflammation remains unclear. In this study, inflammatory response was firstly explored, and its potential proposed. Immunohistochemical staining showed that levels were diminished inflamed rat tissues. vitro, expression significantly down-regulated HDPCs following TNF-α challenge concentration-dependent way, which reached lowest level at 10 ng/ml TNF-α. Such decrease could reversed by MG132, proteasome inhibitor. Unlike BAY 11-7082, NF-κB inhibitor, even reinforced inhibitory effect Quantitative real-time PCR (qRT-PCR) enzyme-linked immunosorbent assay (ELISA) used investigate HDPCs. TNF-α-induced pro-inflammatory cytokines, interleukin (IL)-1β IL-6, lessened when overexpressed Conversely, knockdown exacerbated cytokines. Moreover, Western blot, dual-luciferase reporter assay, immunofluorescence staining, qRT-PCR ELISA results participated NF-κB-dependent manner. These findings suggested defensive inflammation, serving as target exploited for intervention