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Saponin-rich fraction from Clematis chinensis Osbeck roots protects rabbit chondrocytes against nitric oxide-induced apoptosis via preventing mitochondria impairment and caspase-3 activation

机译:威灵仙Osbeck根中富含皂素的组分通过防止线粒体损伤和caspase-3活化来保护兔软骨细胞免受一氧化氮诱导的凋亡

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摘要

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.
机译:我们先前的研究报道,来自铁线莲Osbeck根(SFC)的富含皂苷的部分可通过保护关节软骨和抑制局部炎症有效减轻碘乙酸单钠诱导的大鼠实验性骨关节炎。本研究旨在探讨SFC对关节软骨细胞的预防作用,并探讨其潜在机制。培养原代兔软骨细胞,并使其暴露于NO供体硝普钠(SNP)中。用不同浓度的SFC(30、100、300、1,000μg/ ml)处理24小时后,检查了软骨细胞的核酸形态,凋亡率,线粒体功能和caspase-3活性。结果表明,SNP能诱导家兔软骨细胞发生明显的凋亡,Hoechst 33258染色和流式细胞仪分析证明,SFC以浓度依赖的方式阻止了其凋亡。进一步的研究表明,SFC可以防止经SNP处理的软骨细胞中线粒体膜电位(∆ψm)的去极化并抑制caspase-3的活化。可以得出结论,通过抑制线粒体损伤和caspase-3激活,SFC对关节软骨细胞的保护与抗凋亡作用有关。

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