What question did this study set out to answer?

This research aims to explore how syringin affects osteoclast differentiation, particularly through the regulation of PTGS1 in postmenopausal osteoporosis.

July 26, 2026Discovery Medicine0 citationsOpen Access

Unlocking Bone Health: How Syringin Inhibits Osteoclasts via PTGS1 in Postmenopausal Osteoporosis

Q(Qi Zhang (28502)Guangdong University of Technology YYYanhua YangShanghai Jiao Tong University JHJinhua HuTongji University

Puntos clave

This research aims to explore how syringin affects osteoclast differentiation, particularly through the regulation of PTGS1 in postmenopausal osteoporosis.
RAW 264.7 cells were stimulated with RANKL and treated with varying concentrations of syringin.
Ovariectomized rat model was used to assess the in vivo effects of syringin on bone health.
Quantitative reverse transcription PCR and Western Blot were utilized to measure gene and protein expressions.
Syringin significantly inhibited RANKL-induced osteoclast differentiation and reduced PTGS1 expression (p < 0.01).
In the rat model, syringin increased femoral density (p < 0.01) and reduced serum biomarkers TRAP and ALP (p < 0.05).
PTGS1 overexpression partially reversed the inhibitory effects of syringin, supporting its regulatory role in osteoclast differentiation (p < 0.05).

Resumen

Background: Postmenopausal osteoporosis (PMOP) is a common metabolic bone disease resulting from excessive osteoclast activity, characterized by reduced bone mineral density and increased fracture risk. Syringin (SRG), a natural phenylpropanoid glycoside, has shown potential anti-osteoporotic effects; however, its molecular mechanism remains unclear. This study investigated whether SRG inhibits osteoclast differentiation through regulating prostaglandin-endoperoxide synthase 1 (PTGS1).Methods: RAW 264.7 cells were induced with receptor activator of nuclear factor-κB ligand (RANKL) and treated with SRG at 0, 2.5, 5, and 10 μM. Osteoclast differentiation was evaluated by tartrate-resistant acid phosphatase (TRAP) staining and F-actin ring staining. The mRNA levels of cathepsin K (CTSK), matrix metalloproteinase-9 (Mmp9), and nuclear factor of activated T cells 1 (NFATc1) were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and PTGS1 (also known as COX1) protein expression was detected by Western Blot (WB). PTGS1 expression was regulated to assess its role in SRG-mediated effects. In vivo, an ovariectomized (OVX) rat model was established, and SRG was administered orally at 25 and 50 mg/kg for 8 weeks. Bone mineral density, serum biomarkers (TRAP, alkaline phosphatase ALP, alanine aminotransferase ALT, aspartate aminotransferase AST), and femoral histopathology were analyzed.Results: SRG significantly inhibited RANKL-induced osteoclast differentiation, accompanied by reduced expression of PTGS1, CTSK, Mmp9 and NFATc1 (p < 0.01). PTGS1 overexpression partially reversed these inhibitory effects of SRG (p < 0.05), supporting the involvement of PTGS1 in SRG-mediated regulation of osteoclast differentiation. In the OVX-induced PMOP rat model, SRG treatment increased femoral density (p < 0.01), reduced serum levels of TRAP, ALP and AST (p < 0.05), and improved bone tissue structure.Conclusion: SRG effectively inhibits osteoclast differentiation and mitigates OVX-induced osteoporosis via PTGS1, positioning it as a potential candidate compound for PMOP.

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