ArticleCell proliferation2024
IKK/NF-κB and ROS signal axes are involved in Tenacissoside H mediated inhibitory effects on LPS-induced inflammatory osteolysis.
Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Protective Effects of Nongxiang-TypeFood science & nutrition · 2026Article
- PDLSC-CM targets HAPLN1 in macrophages to reduce root resorption in delayed replanted teeth.Stem cell research & therapy · 2026Article
- Hypoxia Exacerbates Periapical Periodontitis-Associated Pathological Bone Loss via the Hypoxia-Inducible Factor-2α-Calmodulin-Dependent Protein Kinase IV Axis.Cell proliferation · 2026Article
- DNA framework-based nanomedicine platform: a triple-function strategy for treating periodontitis via antibacterial, anti-inflammatory, and osteogenesis-promoting activities.International journal of oral science · 2026Article
- Cuproptosis promotes inflammatory osteolysis via GYS1-mediated glycogen metabolism.International journal of oral science · 2026Article
- Research progress on the intervention of osteoporosis by Chinese herbal monomers based on the Nrf2/NF-κB/MAPK pathway.Frontiers in endocrinology · 2026Review
- IKK/NF-κB Inactivation by Salidroside via Targeting TNF-α for the Treatment of LPS-Induced Colitis.Current issues in molecular biology · 2025Article
- Targeting Irgm1 to combat osteoporosis: suppressing ROS and restoring bone remodeling.Cell death & disease · 2025Article
- Pinosylvin Inhibits Inflammatory and Osteoclastogenesis via NLRP3 Inflammasome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pharmacological Intervention with 4-Phenylbutyrate Ameliorates TiAl6V4 Nanoparticles-Induced Inflammatory Osteolysis by Promoting Macrophage Apoptosis.Bioengineering (Basel, Switzerland) · 2025Article
- Anthocyanins Delay D-Galactose-Induced Mouse Liver Aging by Regulating the NF-κB/IKK Signaling Pathway.Food science & nutrition · 2025Article
- Quercetagetin alleviates inflammatory osteoclastogenesis and collagen antibody-induced arthritis via Nrf2 signaling and Pten/AKT/Nfatc1 axis.Arthritis research & therapy · 2025Article
- Norwogonin Attenuates Inflammatory Osteolysis and Collagen-Induced Arthritis via Modulating Redox Signalling and Calcium Oscillations.Journal of cellular and molecular medicine · 2025Article
- OTUD1 inhibits osteoclast differentiation and osteoclastic bone loss through deubiquitinating and stabilizing PRDX1.Theranostics · 2025Article
- IKK/NF-κB and ROS signal axes are involved in Tenacissoside H mediated inhibitory effects on LPS-induced inflammatory osteolysis.Cell proliferation · 2024Article
- Huangqin Qingre Chubi Capsule inhibits rheumatoid arthritis by regulating intestinal flora and improving intestinal barrier.Frontiers in pharmacology · 2024Article
- Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Periodontal disease and arthroplasty prosthesis loosening and destabilization are both associated with osteolysis, which is predominantly caused by abnormal bone resorption triggered by pro-inflammatory cytokines. Osteoclasts (OCs) are critical players in the process. Concerns regarding the long-term efficacy and side effects of current frontline therapies, however, remain. Alternative therapies are still required. The aim of this work was to investigate the involvement of Tenacissoside H (TDH) in RANKL-mediated OC differentiation, as well as inflammatory osteolysis and associated processes. In vitro, bone marrow-derived macrophages (BMMs) cultured with RANKL and M-CSF were used to detect TDH in the differentiation and function of OCs. Real-time quantitative PCR was used to measure the expression of specific genes and inflammatory factors in OCs. Western blot was used to identify NFATc1, IKK, NF-κB, MAPK pathway, and oxidative stress-related components. Finally, an LPS-mediated calvarial osteolysis mouse model was employed to explore TDH's role in inflammatory osteolysis. The results showed that in vivo TDH inhibited the differentiation and resorption functions of OCs and down-regulated the transcription of osteoclast-specific genes, as well as Il-1β, Il-6 and Tnf-α. In addition, TDH inhibited the IKK and NF-κB signalling pathways and down-regulated the level of ROS. In vivo studies revealed that TDH improves the bone loss caused by LPS. TDH may be a new candidate or treatment for osteoclast-associated inflammatory osteolytic disease.
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