PUBLICATION
Exploring the potential mechanism of B-phycoerythrin on DSS-induced colitis and colitis-associated bone loss based on network pharmacology, molecular docking, and experimental validation
- Authors
- Deng, L., Feng, Z., Li, X., Fan, L., Wu, X., Tavakoli, S., Zhu, Y., Ye, H., Wu, K.
- ID
- ZDB-PUB-250216-5
- Date
- 2025
- Source
- Scientific Reports 15: 54555455 (Journal)
- Registered Authors
- Keywords
- B-phycoerythrin, Inflammatory bowel disease, Molecular docking, Network pharmacology, Osteoporosis, PI3K/AKT signaling pathway
- MeSH Terms
-
- Network Pharmacology*
- Phosphatidylinositol 3-Kinases/metabolism
- Bone Resorption/drug therapy
- Bone Resorption/metabolism
- Bone Resorption/pathology
- Dextran Sulfate*
- Signal Transduction/drug effects
- Animals
- Molecular Docking Simulation*
- Proto-Oncogene Proteins c-akt/metabolism
- Disease Models, Animal
- Protein Interaction Maps/drug effects
- Colitis*/chemically induced
- Colitis*/complications
- Colitis*/drug therapy
- Colitis*/metabolism
- Colitis*/pathology
- Humans
- Phycoerythrin*/chemistry
- Phycoerythrin*/metabolism
- Zebrafish*
- PubMed
- 39953092 Full text @ Sci. Rep.
Citation
Deng, L., Feng, Z., Li, X., Fan, L., Wu, X., Tavakoli, S., Zhu, Y., Ye, H., Wu, K. (2025) Exploring the potential mechanism of B-phycoerythrin on DSS-induced colitis and colitis-associated bone loss based on network pharmacology, molecular docking, and experimental validation. Scientific Reports. 15:54555455.
Abstract
B-phycoerythrin (B-PE), a pigment protein, has found extensive applications in the food, pharmaceutical, and cosmetic industries. However, the effects and potential mechanisms of B-PE on colitis and colitis-associated bone loss remain unclear. Thus, the aim of this study was to investigate the pharmacological mechanisms of B-PE against colitis and colitis-associated bone loss using network pharmacology analysis, molecular docking, and experimental validation. Based on public databases, 99 common targets of B-PE against inflammatory bowel disease and osteoporosis were predicted. The protein-protein interaction network identified 16 core targets, including TNF, AKT1, EGFR, etc., as hub targets. Additionally, functional enrichment analyses and molecular docking results revealed that the PI3K/AKT signaling pathway may serve as a potential signaling pathway for B-PE in the treatment of colitis and colitis-associated bone loss. Furthermore, pharmacological experiments indicated that B-PE not only reversed the elevated expression of TNF-α, IL-1β, MMP9, and CXCL8a, and the reduced expression of ZO-1, E-cadherin, COL1A1, and RUNX2 in the DSS-induced colitis zebrafish model, but also enhanced the phosphorylation of PI3K and AKT, thereby mitigating inflammatory response and promoting osteogenesis. In conclusion, this study provides a theoretical basis for considering B-PE as a promising candidate for the treatment of colitis and colitis-associated bone loss.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping