PloS one · 2025
Molecular mechanisms of dragon's blood in treating ulcerative colitis based on NF-κb/NLPR3/Caspase-1 pyroptosis signaling pathway.
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Cai Bilian, Qin Xiaohua, Huang Xiaogang, He Xiaojin, Zhong Huanying, Yu Yuan, Cui Jinzhu, Wen Yilei
Аннотация
OBJECTIVE: To elucidate the molecular mechanism of dragon's blood (DB) in the treatment of ulcerative colitis (UC).
METHODS: Bioactive metabolites of DB absorbed into the bloodstream were characterized via LC-MS. Network pharmacology and molecular docking were employed to construct a target-pathway interaction model predicting DB's therapeutic mechanism in UC. A 4% DSS-induced UC mouse model was used for experimental validation.
RESULTS: DB markedly alleviated colonic injury in DSS-induced UC. A total of 255 active compounds were identified, including 6,4'-Dimethoxy-7-hydroxyisoflavone, 7-hydroxy-2-(4-methoxyphenyl) chromen-4-one, and Apigenin. Key molecular targets included NLPR3, MAPK1, TP53, HIF1A, and PTGS2. The NF-κB/NLPR3/Caspase-1 axis was implicated as a central pathway mediating the therapeutic effects of DB.
CONCLUSION: DB acts through a multi-component, multi-target, and multi-pathway strategy. Inhibiting the NF-κB/NLPR3/Caspase-1 pyroptosis pathway positions NLPR3 as a viable target for DB in UC intervention.
METHODS: Bioactive metabolites of DB absorbed into the bloodstream were characterized via LC-MS. Network pharmacology and molecular docking were employed to construct a target-pathway interaction model predicting DB's therapeutic mechanism in UC. A 4% DSS-induced UC mouse model was used for experimental validation.
RESULTS: DB markedly alleviated colonic injury in DSS-induced UC. A total of 255 active compounds were identified, including 6,4'-Dimethoxy-7-hydroxyisoflavone, 7-hydroxy-2-(4-methoxyphenyl) chromen-4-one, and Apigenin. Key molecular targets included NLPR3, MAPK1, TP53, HIF1A, and PTGS2. The NF-κB/NLPR3/Caspase-1 axis was implicated as a central pathway mediating the therapeutic effects of DB.
CONCLUSION: DB acts through a multi-component, multi-target, and multi-pathway strategy. Inhibiting the NF-κB/NLPR3/Caspase-1 pyroptosis pathway positions NLPR3 as a viable target for DB in UC intervention.