Related Experiment Video
Updated: May 21, 2025

Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists
Published on: November 15, 2013
Network analysis and experimental validation analysis reveal the mechanism by which psoralen improves
Wenxiang Zeng1, Ying Zhao2, Qingyu Tu1
1The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China; Hangzhou Xiaoshan Hospital of Traditional Chinese Medicine, Hangzhou 311200, China.
Insights
Psoralen (PSO) may treat glucocorticoid-induced growth retardation (GIGR) in children. This study found PSO enhances growth plate chondrocyte proliferation and bone growth by activating the PI3K/AKT pathway, offering a potential therapeutic strategy.
Area of Science:
- Pharmacology
- Endocrinology
- Cell Biology
Background:
- Glucocorticoids (GCs) are widely used medications with significant side effects, including growth retardation in pediatric patients.
- GC-induced growth retardation (GIGR) negatively impacts skeletal development by inhibiting endochondral ossification in growth plate chondrocytes.
- Psoralen (PSO) has demonstrated potential in preserving cartilage homeostasis and enhancing chondrocyte proliferation, but its mechanisms against GIGR are not fully understood.
Purpose of the Study:
- To investigate the therapeutic potential of psoralen (PSO) in mitigating glucocorticoid-induced growth retardation (GIGR).
- To elucidate the underlying molecular mechanisms by which PSO affects GC-damaged growth plate chondrocytes.
Main Methods:
- Network pharmacology and molecular docking were employed to identify potential therapeutic targets of PSO.
- Experimental validation in a rat model and in vitro cell cultures assessed PSO's effects on growth plate chondrocytes.
- Western blotting and immunofluorescence were used to analyze protein expression and signaling pathway activation.
Main Results:
- PSO treatment significantly increased femoral length and growth plate size in rats compared to controls.
- In vitro studies showed PSO enhances growth plate chondrocyte proliferation and maintains cellular homeostasis.
- PSO activated the PI3K/AKT signaling pathway, increased cartilage-related protein expression, and reduced apoptotic protein levels.
Conclusions:
- Psoralen (PSO) demonstrates a protective effect against GC-induced damage in growth plate chondrocytes.
- PSO promotes skeletal growth and chondrocyte proliferation by activating the PI3K/AKT signaling pathway.
- PSO represents a promising therapeutic candidate for managing GC-induced growth retardation (GIGR).
Abstract:
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.
More Related Videos
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

