4.6 Article

Asperuloside Prevents Peri-Implantitis via Suppression of NF-κB and ERK1/2 on Rats

期刊

PHARMACEUTICALS
卷 15, 期 8, 页码 -

出版社

MDPI
DOI: 10.3390/ph15081027

关键词

asperuloside; peri-implantitis; osteoclasts; NF-kappa B signaling; ERK1/2 signaling

资金

  1. National Key Research and development Program of China [2017YFB1104102]
  2. 2020 Hospital Science and Technology Development Fund [2020JZ081]

向作者/读者索取更多资源

Peri-implantitis is a condition characterized by inflammation and bone resorption, leading to implant failure. Asperuloside (ASP), an iridoid glycoside, has shown significant anti-inflammatory properties and the potential to attenuate peri-implantitis bone resorption. This study found that ASP could inhibit osteoclast formation, decrease pro-inflammatory cytokine levels, and mitigate bone resorption in peri-implantitis.
Peri-implantitis is characterized by inflammatory cell infiltration and hyperactivation of the osteoclasts surrounding dental implants which can result in bone resorption and ultimately implant failure. Therefore, coordinating the activity of inflammatory response and bone-resorbing osteoclasts is crucial for the prevention of peri-implantitis. Asperuloside (ASP), an iridoid glycoside, has significant anti-inflammatory activities, suggesting the great potential in attenuating peri-implantitis bone resorption. A ligature-induced peri-implantitis model in the maxilla of rats was established, and the effects of ASP on preventing peri-implantitis were evaluated after four weeks of ligation using micro-CT and histological staining. RT-PCR, western blotting, tartrate-resistant acid phosphatase (TRAP), and immunofluorescent staining were conducted on osteoclasts to confirm the mechanisms of ASP on osteoclastogenesis. The results show that ASP could lead to attenuation of alveolar bone resorption in peri-implantitis by inhibiting osteoclast formation and decreasing pro-inflammatory cytokine levels in vivo. Furthermore, ASP could inhibit osteoclastogenesis by downregulating expression levels of transcription factors nuclear factor of activated T-cell (NFATc1) via restraining the activations of nuclear factor kappa beta (NF-kappa B) and the phosphorylation of extracellular signal-related kinase 1/2 (ERK1/2). In conclusion, ASP could significantly attenuate bone resorption in peri-implantitis via inhibition of osteoclastogenesis by suppressing NF-kappa B and ERK1/2 signaling pathways activations.

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