1. Protective effects and regulatory mechanisms of Platycodin D against LPS-Induced inflammatory injury in BEAS-2B cells.
- Author
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Li W, Zhang Y, Cao Y, Zhao X, and Xie J
- Subjects
- Humans, Cell Line, Oxidative Stress drug effects, Mitochondria drug effects, Mitochondria metabolism, Molecular Docking Simulation, NLR Family, Pyrin Domain-Containing 3 Protein metabolism, Inflammation drug therapy, Inflammation chemically induced, Reactive Oxygen Species metabolism, Saponins pharmacology, Saponins therapeutic use, Lipopolysaccharides, Triterpenes pharmacology, Triterpenes therapeutic use, Platycodon chemistry, Anti-Inflammatory Agents pharmacology, Anti-Inflammatory Agents therapeutic use, Apoptosis drug effects, Autophagy drug effects
- Abstract
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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)
- Published
- 2024
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