β-谷甾醇通过抑制铁死亡保护人软骨细胞免受IL-1β诱导的损伤
β-Sitosterol protects human chondrocytes from IL-1β -induced damage by inhibiting ferroptosis.
摘要(中文译文)
为探究β-谷甾醇对白细胞介素（IL）-1β诱导的软骨细胞损伤的作用及其相关机制，采用IL-1β处理永生化人软骨细胞构建骨关节炎模型。在细胞实验前，通过FTIR、H NMR、C NMR、RP-HPLC-ELSD和UPLC-MS确认β-谷甾醇的身份和纯度。通过qPCR和CCK8实验确定IL-1β和β-谷甾醇处理细胞的最佳浓度。将细胞分为三组：对照组、模型组和模型+β-谷甾醇组。通过CCK8实验检测细胞活力。通过qPCR检测IL-18、IL-1β和肿瘤坏死因子-α（TNF-α）的mRNA表达。通过免疫荧光检测II型胶原α1链（COL2A1）和基质金属蛋白酶13（MMP13）的表达。通过流式细胞术检测活性氧（ROS）和线粒体膜电位。通过ELISA和生化检测检测丙二醛（MDA）、谷胱甘肽（GSH）和铁（Fe）含量。通过透射电子显微镜观察线粒体结构，通过Western blot检测铁死亡相关因子的蛋白表达。IL-1β诱导软骨细胞后，细胞活力下降，炎症细胞因子的基因表达升高，ROS含量降低的细胞比例和线粒体膜电位降低的细胞比例增加，MDA和Fe含量增加，GSH含量降低。线粒体结构呈现铁死亡样改变。COL2A1、谷胱甘肽过氧化物酶4（GPX4）、溶质载体家族7成员11（SLC7A11）、总核因子红细胞2相关因子2（NRF2）及核内NRF2的表达降低。MMP13、ANO6和p-p38/p38水平升高。β-谷甾醇处理软骨细胞可逆转IL-1β诱导的这些变化。经光谱确认的高纯度β-谷甾醇通过抑制炎症激活、细胞外基质降解、线粒体功能障碍和铁死亡相关氧化损伤，减轻IL-1β诱导的软骨细胞损伤，提示其作为骨关节炎干预候选化合物的潜力。
Abstract
To investigate the effect of β-Sitosterol on interleukin (IL)-1β-induced chondrocyte injury and the related mechanism. An osteoarthritis model was constructed by treating immortalized human cartilage cells with IL-1β. The identity and purity of β-Sitosterol were confirmed by FTIR, H NMR, C NMR, RP-HPLC-ELSD, and UPLC-MS before cell experiments. The optimal concentrations of IL-1β and β-Sitosterol for treating cells were determined by qPCR and CCK8 assay. The cells were divided into three groups: Control group, Model group, and Model+β-Sitosterol group. Cell viability was detected by CCK8 assay. The mRNA expression of IL-18, IL-1β and tumor necrosis factor-α (TNF-α) was detected by qPCR. Collagen type II alpha 1 chain (COL2A1) and matrix metalloproteinase 13 (MMP13) expression was detected by immunofluorescence. Reactive oxygen species (ROS) and mitochondrial membrane potential were detected by flow cytometry. Malondialdehyde (MDA), Glutathione (GSH) and Fe were detected by ELISA and biochemical test. Mitochondrial structure was observed by transmission electron microscopy, and the protein expression of ferroptosis related factors was detected by Western blot. After induction of chondrocytes with IL-1β, the cell viability was decreased, the gene expression of inflammatory cytokines was increased, the proportion of cells with reduced ROS content and mitochondrial membrane potential were increased, MDA and Fe content were increased, and GSH content was decreased. Mitochondrial structure showed ferroptosis-like changes. The expression of COL2A1, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), total nuclear factor erythroid 2-related factor 2 (NRF2), and nuclear NRF2 was decreased. MMP13, ANO6, and p-p38/p38 levels were increased. Treatment of chondrocytes with β-Sitosterol could reverse these changes induced by IL-1β. Spectrally confirmed, high-purity β-Sitosterol alleviated IL-1β-induced chondrocyte injury by suppressing inflammatory activation, extracellular matrix degradation, mitochondrial dysfunction, and ferroptosis-related oxidative damage, suggesting its potential as a candidate compound for osteoarthritis intervention.
如何引用
AMA
Le Zhang, Xiaochuan Kong, Gang Hong, Yinfeng Zheng, Lei Zang. β-Sitosterol protects human chondrocytes from IL-1β -induced damage by inhibiting ferroptosis.. Biochemical and biophysical research communications. 2026; doi:10.1016/j.bbrc.2026.154096.
APA
Le Zhang, Xiaochuan Kong, Gang Hong, Yinfeng Zheng, Lei Zang (2026). β-Sitosterol protects human chondrocytes from IL-1β -induced damage by inhibiting ferroptosis.. Biochemical and biophysical research communications. https://doi.org/10.1016/j.bbrc.2026.154096
GB/T 7714
Le Zhang, Xiaochuan Kong, Gang Hong, Yinfeng Zheng, Lei Zang. β-Sitosterol protects human chondrocytes from IL-1β -induced damage by inhibiting ferroptosis.[J]. Biochemical and biophysical research communications, 2026 doi:10.1016/j.bbrc.2026.154096.
在 PubMed增强版 阅读全文
翻译全文 · AI 文献问答 · PDF 原文下载 · 引用导出