Journal of ethnopharmacology · 2026
Research on the mechanism of Carthamus tinctorius L. against skin fibrosis in systemic sclerosis based on serum pharmacochemistry, network pharmacology, and experimental validation.
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Ping Xingfeng, Zhang Yilin, Zhang Jiajia, Wang Ke, Wang Chao, Li Kai, Huang Zongxuan, Lv Junying
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Carthamus tinctorius L., a plant prominently used in Traditional Chinese Medicine, has been effectively applied clinically for treatment of systemic sclerosis (SSc). Our previous studies have indicated that Carthamus tinctorius L. has therapeutic potential for the treatment of SSc; however, detailed mechanisms remain unclear.
OBJECTIVE: This study seeks to determine the active components of Carthamus tinctorius L., assess its impact on skin fibrosis in SSc, and investigate potential targets and antifibrotic mechanisms.
METHODS: Ultra-High Performance Liquid Chromatography-Quadrupole-Time-of-Flight Mass Spectrometry (UHPLC-Q-TOF-MS) was used to characterize the primary bioactive compounds in Carthamus tinctorius L. The therapeutic targets and associated pathways relevant to SSc were subsequently predicted by integrating network pharmacology with molecular docking, followed by rigorous validation in both in vivo and in vitro experimental systems.
RESULTS: Using UHPLC-Q-TOF-MS, we identified 218 active constituents in Carthamus tinctorius L., 7 of which were found to enter the bloodstream. Further, network pharmacology predicted 90 potential targets, primarily linked to the Phosphoinositide 3-kinase-Protein Kinase B (PI3K-AKT) signaling pathway. Molecular docking revealed that the key active component kaempferol can stably bind to AKT1, PIK3CA, PIK3R1, and other target proteins. In vivo experiments showed that treatment with Carthamus tinctorius L. enhances autophagy and apoptosis, alleviating skin fibrosis in SSc mice. In vitro studies confirmed that kaempferol promotes cellular autophagy and apoptosis, reduces the expression of fibrotic markers and oxidative stress levels, and inhibits phosphorylation of PI3K/AKT pathway-related proteins.
CONCLUSION: This study demonstrates that Carthamus tinctorius L. can alleviate the degree of skin fibrosis and improve pathological skin structure in SSc. It further clarifies that its key active ingredient, kaempferol, inhibits the PI3K/AKT/mTOR signaling pathway, thereby promoting cellular autophagy and inducing apoptosis, ultimately suppressing the fibrotic process in human skin fibroblasts. These findings provide new experimental evidence and research perspectives for elucidating the pharmacological mechanism by which Carthamus tinctorius L. exerts antifibrotic effects.
OBJECTIVE: This study seeks to determine the active components of Carthamus tinctorius L., assess its impact on skin fibrosis in SSc, and investigate potential targets and antifibrotic mechanisms.
METHODS: Ultra-High Performance Liquid Chromatography-Quadrupole-Time-of-Flight Mass Spectrometry (UHPLC-Q-TOF-MS) was used to characterize the primary bioactive compounds in Carthamus tinctorius L. The therapeutic targets and associated pathways relevant to SSc were subsequently predicted by integrating network pharmacology with molecular docking, followed by rigorous validation in both in vivo and in vitro experimental systems.
RESULTS: Using UHPLC-Q-TOF-MS, we identified 218 active constituents in Carthamus tinctorius L., 7 of which were found to enter the bloodstream. Further, network pharmacology predicted 90 potential targets, primarily linked to the Phosphoinositide 3-kinase-Protein Kinase B (PI3K-AKT) signaling pathway. Molecular docking revealed that the key active component kaempferol can stably bind to AKT1, PIK3CA, PIK3R1, and other target proteins. In vivo experiments showed that treatment with Carthamus tinctorius L. enhances autophagy and apoptosis, alleviating skin fibrosis in SSc mice. In vitro studies confirmed that kaempferol promotes cellular autophagy and apoptosis, reduces the expression of fibrotic markers and oxidative stress levels, and inhibits phosphorylation of PI3K/AKT pathway-related proteins.
CONCLUSION: This study demonstrates that Carthamus tinctorius L. can alleviate the degree of skin fibrosis and improve pathological skin structure in SSc. It further clarifies that its key active ingredient, kaempferol, inhibits the PI3K/AKT/mTOR signaling pathway, thereby promoting cellular autophagy and inducing apoptosis, ultimately suppressing the fibrotic process in human skin fibroblasts. These findings provide new experimental evidence and research perspectives for elucidating the pharmacological mechanism by which Carthamus tinctorius L. exerts antifibrotic effects.