Pakistan journal of pharmaceutical sciences · 2026
Mechanisms of Quyu tong-bi decoction for the treatment of type III prostatitis - based on database and in-vitro experiments.
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Ma Miaomiao, Wang Zulong, Ju Baojun
Аннотация
BACKGROUND: Quyu tong-bi decoction (QYTB) has demonstrated significant clinical efficacy in treating type III prostatitis. However, its underlying pharmacological mechanisms remain to be fully elucidated.
OBJECTIVES: This study aimed to investigate the molecular mechanisms by which QYTB addresses type III prostatitis by integrating network pharmacology, molecular docking and experimental validation.
METHODS: Active ingredients and potential targets of QYTB were retrieved from the TCMSP and UniProt databases. Disease-associated targets for type III prostatitis were collected from GeneCards, OMIM and TTD. After identifying drug-disease intersection targets, protein-protein interaction (PPI) networks and topological analyses were performed using Cytoscape and STRING. GO and KEGG enrichment analyses were conducted via Metascape. Finally, molecular docking and in-vitro experiments using SP-induced rat spinal cord astrocytes were performed for validation.
RESULTS: Thirty-two core targets of QYTB were identified, primarily involving oxidative stress, inflammatory response and apoptosis. In-vitro validation revealed that QYTB-containing serum notably upregulated the concentrations of CAT, SOD and GSH in SP-induced astrocytes while reducing MDA levels. Furthermore, QYTB downregulated pro-inflammatory markers (IL-6, TNF-α and IL-1β) and suppressed the phosphorylation of p38MAPK and CREB within the MAPK signaling pathway.
CONCLUSION: QYTB exerts potent antioxidant and anti-inflammatory effects in the treatment of type III prostatitis, likely through the modulation of the MAPK signaling pathway.
OBJECTIVES: This study aimed to investigate the molecular mechanisms by which QYTB addresses type III prostatitis by integrating network pharmacology, molecular docking and experimental validation.
METHODS: Active ingredients and potential targets of QYTB were retrieved from the TCMSP and UniProt databases. Disease-associated targets for type III prostatitis were collected from GeneCards, OMIM and TTD. After identifying drug-disease intersection targets, protein-protein interaction (PPI) networks and topological analyses were performed using Cytoscape and STRING. GO and KEGG enrichment analyses were conducted via Metascape. Finally, molecular docking and in-vitro experiments using SP-induced rat spinal cord astrocytes were performed for validation.
RESULTS: Thirty-two core targets of QYTB were identified, primarily involving oxidative stress, inflammatory response and apoptosis. In-vitro validation revealed that QYTB-containing serum notably upregulated the concentrations of CAT, SOD and GSH in SP-induced astrocytes while reducing MDA levels. Furthermore, QYTB downregulated pro-inflammatory markers (IL-6, TNF-α and IL-1β) and suppressed the phosphorylation of p38MAPK and CREB within the MAPK signaling pathway.
CONCLUSION: QYTB exerts potent antioxidant and anti-inflammatory effects in the treatment of type III prostatitis, likely through the modulation of the MAPK signaling pathway.