ArticleDrug design, development and therapy2021
Inhibition of Lipopolysaccharide-Induced Inflammatory Bone Loss by Saikosaponin D is Associated with Regulation of the RANKL/RANK Pathway.
Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Microbial messengers: decoding the gut microbiota's role in bone health through immunomodulation and exosomal signaling.NPJ biofilms and microbiomes · 2026Review
- Research Progress of Treatment of Gouty Arthritis with Chinese Medicine Based on Signal Pathways.Chinese journal of integrative medicine · 2026Review
- The role of the neuro-immune-bone axis in osteoporosis: from bone remodeling imbalance to multi-system interactions.Frontiers in immunology · 2026Review
- Cyclin-dependent kinase inhibitor-1 deficiency enhances bone destruction in a mouse model of arthritis.Bone reports · 2025Article
- Human umbilical cord mesenchymal stem cells secretome and nanoemulsion propolis combination ameliorate osteoclastogenesis in lipopolysaccharide-induced osteolysis in hyperglycemia rats.Journal of dental sciences · 2025Article
- Self-powered intracellular nanogenerator attenuates inflammatory osteolysis through mitochondrial MRS2/MgMaterials today. Bio · 2025Article
- Ultrasound-Responsive Piezoelectric Membrane Promotes Osteoporotic Bone Regeneration via the "Two-Way Regulation" Bone Homeostasis Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- IL13Rα2 as a crucial receptor for Chi3l1 in osteoclast differentiation and bone resorption through the MAPK/AKT pathway.Cell communication and signaling : CCS · 2024Article
- Article
- Non-Alcoholic Fatty Liver Disease and Bone Tissue Metabolism: Current Findings and Future Perspectives.International journal of molecular sciences · 2023Review
- Small extracellular vesicles derived from hypoxic preconditioned dental pulp stem cells ameliorate inflammatory osteolysis by modulating macrophage polarization and osteoclastogenesis.Bioactive materials · 2023Article
- Review
- Gut-spine axis: a possible correlation between gut microbiota and spinal degenerative diseases.Frontiers in microbiology · 2023Review
- Mechanism of regulating macrophages/osteoclasts in attenuating wear particle-induced aseptic osteolysis.Frontiers in immunology · 2023Review
- Piperlongumine Inhibits Titanium Particles-Induced Osteolysis, Osteoclast Formation, and RANKL-Induced Signaling Pathways.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteolytic diseases such as osteoporosis are featured with accelerated osteoclast differentiation and strong bone resorption. Considering the complications and other limitations of current drug treatments, it is necessary to develop a safer and more reliable drug to deal with osteoclast-related diseases. Saikosaponin D (SSD) is the active extract of Bupleurum, which has anti-inflammation, anti-tumor and liver protection functions. However, the role of SSD in regulating the differentiation and function of osteoclasts is not clear. PURPOSE: To explore whether SSD could prevent osteoclast differentiation and bone resorption induced by M-CSF and RANKL, and further evaluate the potential therapeutic properties of SSD in LPS-induced inflammatory bone loss mouse models.
methodsBMMs were cultured in complete medium stimulated by RANKL with different concentrations of SSD. TRAP staining, bone resorption determination, qRT-PCR, immunofluorescence and Western blotting were performed. A mouse model of LPS-induced calvarial bone loss was established and treated with different doses of SSD. The excised calvaria bones were used for TRAP staining, micro-CT scan and histological analysis.
resultsSSD inhibited the formation and bone resorption of osteoclasts induced by RANKL in vitro. SSD suppressed LPS-induced inflammatory bone loss in vivo.
conclusionSSD inhibited osteoclastogenesis and LPS-induced osteolysis in mice both which served as a new potential agent for the treatment of osteoclast-related conditions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.