ArticlePhytotherapy research : PTR2025
Salvianolic Acid A Mitigates Osteoporotic Bone Loss by Repressing Reactive Oxygen Species via the Nrf2-HO-1 Pathway.
Article in Phytotherapy research : PTR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pharmacological effects ofFrontiers in pharmacology · 2026Pooled it
- Research trends and hotspots in osteoporosis associated with gas molecules and related factors: a bibliometric analysis.Medical gas research · 2026Article
- Heme Oxygenase-1 in Bone Remodeling: Molecular Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Design, Synthesis and Biological Evaluation of Novel Furanocoumarin Derivatives: Validation of Anti-Osteoporotic Efficacy In Vitro and In Vivo.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Uridine inhibits ROS-mediated osteoclast differentiation and alleviates osteoporosis via modulation of PI3K/Akt-FoxO signaling.Frontiers in immunology · 2026Article
- Salvianolic Acid A Mitigates Osteoporotic Bone Loss by Repressing Reactive Oxygen Species via the Nrf2-HO-1 Pathway.Phytotherapy research : PTR · 2025Article
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Authors and funding
6 authors.
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Abstract
Osteoporosis, characterized by osteoclastic bone resorption, has been the focus of research. Studies implicate that reactive oxygen species (ROS) accumulate intracellularly during osteoclastogenesis. Salvianolic acid A (SAA), a compound derived from Salvia miltiorrhiza, has been widely used to treat cardiovascular and cerebrovascular disorders, owing to its antioxidant and anti-inflammatory properties. In this study, we investigated the therapeutic effects of SAA on osteoporotic bone loss in vitro and in osteoporotic mice induced by ovariectomy (OVX) and explored the underpinning mechanisms. In vitro, SAA significantly restrained osteoclastogenesis and osteoclastic resorption in a dose- and time-dependent manner. SAA markedly blocked the expression of osteoclast-specific genes and proteins such as NFATc1 and c-Fos. Specifically, SAA reduced ROS production by enhancing the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to activate HO-1 and catalase, with no effect on Bach1. In addition, SAA simultaneously suppressed the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathway, ultimately arresting NFATc1 expression to constrain the differentiation and function of osteoclasts. Micro-CT and histological evidence demonstrated that SAA at a nontoxic dose successfully reduced bone loss induced by OVX, with fewer mature osteoclasts. These findings revealed that SAA provides a potential treatment strategy for reducing osteoclast-related bone ailments, including osteoporosis.
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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 Socratic graph.