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Network analysis and experimental validation analysis reveal the mechanism by which psoralen improves glucocorticoid-induced growth retardation
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DOI：10.1016/j.jpba.2025.116801.png)
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Abstract
En 中文
Glucocorticoids (GCs) are widely used, particularly concerning in pediatric patients. GC-induced growth retardation (GIGR) is one of its significant side effects. Endochondral ossification of growth plate chondrocytes is crucial for skeletal growth in children; excessive GCs inhibit growth plate development and longitudinal bone growth. Previous studies have shown that psoralen (PSO) has anti-osteoporotic effects, preserves cartilage homeostasis, and enhances chondrocyte proliferation. However, the specific mechanisms remain unclear. This study used network pharmacology and molecular docking to identify targets, followed by experimental validation to investigate how PSO affects damage to GC-induced growth plate chondrocytes. Results show that the PSO group exhibited significant increases in femoral length and growth plate size compared to the model group in rats. Additionally, testicular weight significantly increased in the PSO group compared to the model group. In vitro experiments demonstrated that PSO enhances proliferation and maintains cellular homeostasis in growth plate chondrocytes. Furthermore, experiments employing Western blotting, immunofluorescence, and other methods confirmed increased PI3K/AKT pathway activity, as well as elevated expression of cartilage-related proteins and reduced apoptotic proteins. Through network pharmacology, molecular docking, and experimental validation, we found that PSO stabilizes growth plate cell homeostasis and promotes cell proliferation by activating the PI3K/AKT signaling pathway. Therefore, PSO may be a potential therapeutic agent for improving GC-induced GIGR.
Keywords:
Glucocorticoid
Growth retardation
Psoralen
Network pharmacology
Molecular docking
PI3K/AKT pathway
Journal
IF:
3.1
Papers:
1.5W
Citations:
2.5W