ArticleHeliyon2022
Experimental study on the effects of simvastatin in reversing the femoral metaphyseal defects induced by sodium valproate in normal and ovariectomized rats.
Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- The effects of simvastatin on the bone microstructure and mechanics of ovariectomized mice: a micro-CT and micro-finite element analysis study.BMC musculoskeletal disorders · 2024Article
- Trichostatin A enhances the titanium rods osseointegration in osteoporotic rats by the inhibition of oxidative stress through activating the AKT/Nrf2 pathway.Scientific reports · 2023Article
- Aloe polysaccharide promotes osteogenesis potential of adipose-derived stromal cells via BMP-2/Smads and prevents ovariectomized-induced osteoporosis.Molecular biology reports · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Long-term treatment with antiepileptic drugs may cause secondary osteoporosis. The present study investigated the influence of simvastatin (SIM) in reversing the effects of valproate on bone defect healing in normal and ovariectomized (OVX) rats. Methods: Bone defects in femora were established in seven experimental groups of rats: control (vehicle), sodium valproate (SVP; 300 mg/kg/d), SVP plus SIM (25 mg/kg/d), sham control (sham), OVX, OVX SVP and OVX SVP plus SIM. All rats were euthanized at 8 weeks after bone defect creation. Results: Micro-CT, biomechanical and histological evaluations demonstrated lower bone strength and delayed bone healing in the SVP therapy group compared with the SVP plus SIM therapy group. Biochemical and immunohistochemical results showed that osteocalcin (OCN), collagen I (Col I) and procollagen type I N-terminal propeptide (P1NP) levels decreased, tartrate-resistant acid phosphatase type 5 precursor (TRACP-5b) expression increased, and Dickkopf-1 (DKK-1) and receptor activator of nuclear factor-κ B ligand (RANKL) expression were upregulated in the SVP therapy rats compared with the SVP plus SIM therapy group. Bone loss was exacerbated by OVX, but the effect of SIM in ameliorating bone loss was also more marked in the OVX rats. Conclusions: This study indicated lower bone strength and delayed healing of bone defects in rats given SVP therapy, especially the OVX SVP treatment group. In contrast, treatment with SIM was effective in enhancing bone strength and promoting bone defect repair and showed significant influence on promoting osteogenesis and inhibiting osteoclastogenesis.
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Registered trials
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