期刊
MEDIATORS OF INFLAMMATION
卷 2018, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2018/8167932
关键词
-
资金
- National Natural Science Foundation of China [81600904]
- Department of Science and Technology of Guangdong Province [2016ZC0147, 2015110-13]
- Bureau of Science and Technology and Information Technology, Liwan District, Guangzhou City [20151217094]
- Dr. Start-up Fund of Guangzhou Medical University [2015C43]
- Ministry of Science and Technology in Guangzhou, Liwan District [201704048]
Proinflammatory responses are important aspects of the immune response to biomaterials, which may cause peri-implantitis and implant shedding. The purpose of this study was to test the cytotoxicity and proinflammatory effects of dicalcium silicate particles on RAW 264.7 macrophages and to investigate the proinflammatory response mechanism induced by C2S and tricalcium phosphate (TCP). C2S and TCP particles were characterized using scanning electron microscopy (SEM), energy spectrum analysis (EDS) and X-ray diffraction (XRD). Cytotoxicity and apoptosis assays with C2S and TCP in the murine RAW 264.7 cell line were tested using the cell counting kit-8 (CCK-8) assay and flow cytometry (FCM). The detection results showed that C2S and TCP particles had no obvious toxicity in RAW 264.7 cells and did not cause obvious apoptosis, although they both caused an oxidative stress response by producing ROS when the concentrations were at 100 mu g/mL. C2S particles are likely to induce a proinflammatory response by inducing high TLR2, TNF-alpha mRNA, TNF-alpha proinflammatory cytokine, p-I kappa B, and p-JNK1 + JNK2 + JNK3 expression levels. When we added siRNA-TLR2-1, a significant reduction was observed. These findings support the theory that C2S particles induce proinflammatory responses through the TLR2-mediated NF-kappa B and JNK pathways in the murine RAW 264.7 macrophage cell line.
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