ArticleCytotechnology2013
Saponin-rich fraction from Clematis chinensis Osbeck roots protects rabbit chondrocytes against nitric oxide-induced apoptosis via preventing mitochondria impairment and caspase-3 activation.
Article in Cytotechnology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Widely Targeted Metabolomic Analysis of Metabolic Differences Among Various Organs ofMetabolites · 2026Article
- The Protective Effect ofGenetics research · 2022Article
- Nitrite exposure may induce infertility in mice.Journal of toxicologic pathology · 2022Article
- Therapeutic Single Compounds for Osteoarthritis Treatment.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Asiaticoside Attenuates Cell Growth Inhibition and Apoptosis Induced by AβFrontiers in pharmacology · 2018Article
- Effect of saponin on erythrocytes.International journal of hematology · 2014Article
- Article
- Daphnoretin-induced apoptosis in HeLa cells: a possible mitochondria-dependent pathway.Cytotechnology · 2014Article
- Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats.PloS one · 2013Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study reported that the saponin-rich fraction from Clematis chinensis Osbeck roots (SFC) could effectively alleviate experimental osteoarthritis induced by monosodium iodoacetate in rats through protecting articular cartilage and inhibiting local inflammation. The present study was performed to investigate the preventive effects of SFC on articular chondrocyte, and explore the underlying mechanisms. Primary rabbit chondrocytes were cultured and exposed to sodium nitroprusside (SNP), a NO donor. After treatment with different concentrations of SFC (30, 100, 300, 1,000 μg/ml) for 24 h, nucleic morphology, apoptotic rate, mitochondrial function and caspase-3 activity of chondrocytes were examined. The results showed that SNP induced remarkable apoptosis of rabbit chondrocytes evidenced by Hoechst 33258 staining and flow cytometry analysis, and SFC prevented the apoptosis in a concentration-dependent manner. Further studies indicated that SFC could prevent the depolarization of mitochondrial membrane potential (∆ψm) in SNP-treated chondrocytes and suppress the activation of caspase-3. It can be concluded that the protection of SFC on articular chondrocytes is associated with the anti-apoptosis effects via inhibiting the mitochondrion impairment and caspase-3 activation.
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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 OpenQuestion graph.