School of Biotechnology and Food Science, Tianjin University of Commerce, Tianjin 300134, China; School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.
School of Biotechnology and Food Science, Tianjin University of Commerce, Tianjin 300134, China.
Int Immunopharmacol. 2024 Sep 30;139:112782. doi: 10.1016/j.intimp.2024.112782. Epub 2024 Jul 28.
Platycodin D (PLD), a major bioactive component of triterpene saponins found in Platycodon grandiflora, is renowned for its anti-inflammatory and antioxidant properties. This study aims to explore the protective effects and regulatory mechanisms of PLD in an LPS-induced inflammation injury model of BEAS-2B cells. Initially, PLD was identified from Platycodon grandiflora extracts utilizing UPLC-Q-TOF-MS/MS technology. The effects of PLD on the viability, morphology, ROS levels, and inflammatory factors of LPS-induced BEAS-2B cells were then investigated. The results showed that PLD significantly alleviated LPS-induced oxidative stress and inflammatory injury. Further analysis revealed that PLD positively influenced apoptosis levels, mitochondrial morphology, and related gene expression, indicating its potential to mitigate LPS-induced apoptosis and alleviate mitochondrial dysfunction. Using molecular docking technology, we predicted the binding sites of PLD with mitochondrial autophagy protein. Gene expression levels of autophagy-related proteins were measured to determine the impact of PLD on mitochondrial autophagy. Additionally, the study examined whether the mitochondrial autophagy agonists rapamycin (RAPA) could modulate the upregulation of inflammasome-related factors NLRP3 and Caspase-1 in LPS-induced BEAS-2B cells. This was done to evaluate the regulator mechanisms of PLD in pulmonary inflammatory injury. Our findings suggest that PLD's mechanism of action involves the regulation of mitochondrial autophagy, which in turn modulates inflammatory responses.
远志酸（PLD）是桔梗中三萜皂苷的主要生物活性成分，具有抗炎和抗氧化作用。本研究旨在探讨 PLD 在脂多糖（LPS）诱导的 BEAS-2B 细胞炎症损伤模型中的保护作用及其调控机制。首先，利用 UPLC-Q-TOF-MS/MS 技术从桔梗提取物中鉴定出 PLD。然后研究了 PLD 对 LPS 诱导的 BEAS-2B 细胞活力、形态、ROS 水平和炎症因子的影响。结果表明，PLD 显著减轻 LPS 诱导的氧化应激和炎症损伤。进一步分析表明，PLD 可正向影响细胞凋亡水平、线粒体形态和相关基因表达，提示其可减轻 LPS 诱导的细胞凋亡和缓解线粒体功能障碍。利用分子对接技术预测了 PLD 与线粒体自噬蛋白的结合位点。测量自噬相关蛋白的基因表达水平，以确定 PLD 对线粒体自噬的影响。此外，研究还考察了线粒体自噬激动剂雷帕霉素（RAPA）是否能调节 LPS 诱导的 BEAS-2B 细胞中炎症小体相关因子 NLRP3 和 Caspase-1 的上调，以评估 PLD 在肺炎症损伤中的调控机制。研究结果表明，PLD 的作用机制涉及对线粒体自噬的调节，进而调节炎症反应。
