Hydrogen sulfide protects against particle-induced inflammatory response and osteolysis via SIRT1 pathway in prosthesis loosening
| Autor: | Zhenheng Wang, Ming Zhou, Feng Zhu, Yong Wang, Yaozeng Xu, Tongguo Shi, Rongqun Li, Naicheng Liu, Lei Liu, Zhantao Deng, Jiannong Jiang, Li Ni, Ruofu Zhu, Zhidong Wang, Jun Zhou, Huilin Yang, Yixing Tian |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Osteolysis Cell Survival Blotting Western Fluorescent Antibody Technique Calvaria Inflammation Enzyme-Linked Immunosorbent Assay Real-Time Polymerase Chain Reaction Biochemistry 03 medical and health sciences Mice 0302 clinical medicine Sirtuin 1 In vivo Genetics medicine Animals Hydrogen Sulfide Molecular Biology biology Chemistry X-Ray Microtomography medicine.disease In vitro Resorption 030104 developmental biology medicine.anatomical_structure RAW 264.7 Cells biology.protein Cancer research Tumor necrosis factor alpha medicine.symptom 030217 neurology & neurosurgery Biotechnology Signal Transduction |
| Zdroj: | FASEB journal : official publication of the Federation of American Societies for Experimental BiologyREFERENCES. 34(3) |
| ISSN: | 1530-6860 |
| Popis: | Wear debris-induced osteolysis and ensuing aseptic loosening is the main cause of implant failure and revision surgery. Wear debris-induced inflammatory response plays key roles in peri-implant osteolysis. Recently, substantial of evidence suggests that hydrogen sulfide (H2 S), the third gasotransmitter, is a critical player regulating inflammation. However, the role and therapeutic potential of H2 S in wear debris-induced inflammation and osteolysis remains to be defined. In the present study, we investigated the effect of H2 S on wear debris-induced pro-inflammatory cytokines expression and osteolysis in vitro and in vivo. With a slow-releasing H2 S donor GYY4137, our study demonstrated that H2 S attenuated wear debris-induced osteolysis and osteoclastogenesis in murine calvaria resorption models. The expression of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) that stimulated by wear particles were significantly reduced by GYY4137. Further, the level of sirtuin 1 (SIRT1), which possesses anti-inflammation property, was examined in vivo and in macrophages. And we found that wear debris decreased the expression of SIRT1. Cotreated macrophages with GYY4137 in part reversed the decline of SIRT1. More importantly, with the SIRT1 recombinant lentivirus and small interfering RNAs (siRNA) against SIRT1, our data indicated that SIRT1 mediated the inhibitory effects of GYY4137 on wear debris-induced inflammation. Collectively, these results suggested that exogenous H2 S production (via H2 S donors) may represent a potential approach for the treatment of wear particle-induced osteolysis. |
| Databáze: | OpenAIRE |
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