ArticleFrontiers in pharmacology2018
Magnesium Lithospermate B Protects against Lipopolysaccharide-Induced Bone Loss by Inhibiting RANKL/RANK Pathway.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Pooled it
- The Role of Trace Elements and Minerals in Osteoporosis: A Review of Epidemiological and Laboratory Findings.Biomolecules · 2023Review
- Functionalization of TiOMaterials (Basel, Switzerland) · 2022Review
- Yangonin treats inflammatory osteoporosis by inhibiting the secretion of inflammatory factors and RANKL expression.Inflammopharmacology · 2022Article
- Heat-KilledFrontiers in nutrition · 2022Article
- Magnesium Picolinate Improves Bone Formation by Regulation of RANK/RANKL/OPG and BMP-2/Runx2 Signaling Pathways in High-Fat Fed Rats.Nutrients · 2021Article
- Stachydrine prevents LPS-induced bone loss by inhibiting osteoclastogenesis via NF-κB and Akt signalling.Journal of cellular and molecular medicine · 2019Article
- Forsythiaside inhibited titanium particle-induced inflammationRSC advances · 2019Article
- The Natural Product 6-Gingerol Inhibits Inflammation-Associated Osteoclast Differentiation via Reduction of Prostaglandin E₂ Levels.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) can induce bone loss by stimulating bone resorption. Natural compounds have great potential for the treatment of osteolytic bone diseases. Magnesium lithospermate B (MLB) plays an important role in protecting against oxidative damage and also has potential anti-inflammatory pharmacological properties. However, its role in LPS-induced bone loss is still unknown. In the present study, we observed the effects of MLB on LPS-induced bone damage and investigated the possible mechanisms. The bone loss models were established by LPS administration in male Sprague-Dawley rats. MLB (200 mg/kg body weight) was given by subcutaneous injection. MicroCT analysis, biomarker assay, histological examination and immunohistochemical staining were performed at the 8th weeks. In addition, RAW264.7 cells were treated with LPS in the presence or absence of MLB. The osteoclast formation, resorption activity and differentiation-related genes [(receptor activator of nuclear factor kappa-B (RANK), Traf6, Fra-1, and c-src)] expression were evaluated. LPS induced bone loss shown as the decrease in bone volume fraction and trabecular number, and increase in trabecular separation. LPS also markedly enhanced the osteoclast formation and resorption activity compared with the control. MLB significantly abolished the LPS-induced bone microstructure damage (
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