International immunopharmacology · 2025
Investigation of the effects and mechanism of Total Glycosides of paeony against Radiation-Induced brain injury through network Pharmacology, molecular docking and experimental Verification.
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Zhao Zhongfang, He Xiaohan, Gan Lu, Xu Dan, Zhang Taofeng, Wang Hongyu, Cui Zhencun, Zhang Hong, Liu Bin
Аннотация
BACKGROUND: Total glucosides of paeony (TGP), derived from the dried root of Paeonia, is a popular treatment for immune diseases. Radiation induced brain injury (RBI) is a common side effect of brain radiation therapy, but the efficacy of TGP in treating RBI remains uncertain.
PURPOSE: To evaluate the protective effects of TGP against RBI and elucidate its underlying mechanisms using pharmacological network analysis, molecular docking, and experimental validation.
METHODS: The potential targets of TGP and RBI were identified using network pharmacology. Overlapping targets were analyzed for KEGG pathway enrichment and gene ontology (GO) investigations. The therapeutic effectiveness of TGP and the precision of key target genes were assessed in the mouse model of RBI, alongside observations of behavioral changes and experimental techniques.
RESULTS: Network pharmacology identified 43 targets associated with RBI that intersect with TGP. Protein-Protein Interaction (PPI) analysis highlighted key targets, including EGFR, TNF, and IL-6. Experimental outcomes demonstrated that TGP can mitigate oxidative stress damage and inflammation while enhancing memoryand learning abilities in RBI mice. Additionally, TGP dramatically decreased the activation of astrocytes and microglia, as well as the expression of key targets like EGFR, TNF, and IL-6.
CONCLUSION: TGP effectively mitigates RBI by targeting key therapeutic targets such as EGFR, TNF, and IL-6.
PURPOSE: To evaluate the protective effects of TGP against RBI and elucidate its underlying mechanisms using pharmacological network analysis, molecular docking, and experimental validation.
METHODS: The potential targets of TGP and RBI were identified using network pharmacology. Overlapping targets were analyzed for KEGG pathway enrichment and gene ontology (GO) investigations. The therapeutic effectiveness of TGP and the precision of key target genes were assessed in the mouse model of RBI, alongside observations of behavioral changes and experimental techniques.
RESULTS: Network pharmacology identified 43 targets associated with RBI that intersect with TGP. Protein-Protein Interaction (PPI) analysis highlighted key targets, including EGFR, TNF, and IL-6. Experimental outcomes demonstrated that TGP can mitigate oxidative stress damage and inflammation while enhancing memoryand learning abilities in RBI mice. Additionally, TGP dramatically decreased the activation of astrocytes and microglia, as well as the expression of key targets like EGFR, TNF, and IL-6.
CONCLUSION: TGP effectively mitigates RBI by targeting key therapeutic targets such as EGFR, TNF, and IL-6.