World journal of gastroenterology · 2025
Saffron and Calculus bovis combination exerts anti-hepatic fibrotic effect in liver fibrosis rats via the mitogen-activated protein kinases pathway.
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Sun Sheng-Nan, Wang Kun, Xu Ya, Ye Fei, Xia Wei-Na, Wang Zhu-Wei, Liu Fang, He Zi-Xuan, Chen Meng, Du Qing-Hong
Аннотация
BACKGROUND: Liver fibrosis is a global health issue that lacks effective treatments. Tibetan medicine, with a long history, has accumulated rich experience in the treatment of chronic liver diseases. The saffron (Saf) and Calculus bovis (Cal b) combination is among the most commonly used medicines in clinical practice in Tibetan medicine for hepatic disease. Its characteristic therapies and drug compatibility provide unique ideas for the treatment of liver fibrosis and have research value and application potential.
AIM: To investigate the efficacy of the Saf-Cal b therapy in treating liver fibrosis and explored its underlying mechanism.
METHODS: We initially established a carbon tetrachloride-induced rat liver fibrosis model to assess Saf-Cal b's anti-fibrotic effects. Subsequently, we conducted network pharmacology analysis to identify the potential therapeutic targets and pathways of Saf-Cal b in liver fibrosis intervention. Finally, we performed in vivo validation of key regulatory targets.
RESULTS: Saf-Cal b combination therapy exerted superior effects in ameliorating liver fibrosis in model rats compared with Saf or Cal b monotherapy. Through network pharmacology prediction, key targets of the combination were identified. Mechanistic validation revealed that Saf-Cal b inhibited the p38 mitogen-activated protein kinases pathway, which in turn suppressed the transforming growth factor-β/small mother against decapentaplegic pathway. This sequential inhibition led to reduced activation of hepatic stellate cells, a central event in liver fibrosis progression.
CONCLUSION: These findings demonstrate that Saf-Cal b combination therapy is more effective than either monotherapy in alleviating liver fibrosis, with its therapeutic effect mediated through the p38 mitogen-activated protein kinases/transforming growth factor-β/small mother against decapentaplegic signaling axis, providing a potential therapeutic strategy for liver fibrosis.
AIM: To investigate the efficacy of the Saf-Cal b therapy in treating liver fibrosis and explored its underlying mechanism.
METHODS: We initially established a carbon tetrachloride-induced rat liver fibrosis model to assess Saf-Cal b's anti-fibrotic effects. Subsequently, we conducted network pharmacology analysis to identify the potential therapeutic targets and pathways of Saf-Cal b in liver fibrosis intervention. Finally, we performed in vivo validation of key regulatory targets.
RESULTS: Saf-Cal b combination therapy exerted superior effects in ameliorating liver fibrosis in model rats compared with Saf or Cal b monotherapy. Through network pharmacology prediction, key targets of the combination were identified. Mechanistic validation revealed that Saf-Cal b inhibited the p38 mitogen-activated protein kinases pathway, which in turn suppressed the transforming growth factor-β/small mother against decapentaplegic pathway. This sequential inhibition led to reduced activation of hepatic stellate cells, a central event in liver fibrosis progression.
CONCLUSION: These findings demonstrate that Saf-Cal b combination therapy is more effective than either monotherapy in alleviating liver fibrosis, with its therapeutic effect mediated through the p38 mitogen-activated protein kinases/transforming growth factor-β/small mother against decapentaplegic signaling axis, providing a potential therapeutic strategy for liver fibrosis.
Предметные рубрики MeSH
AnimalsRatsMaleCarbon TetrachlorideCrocusLiverMAP Kinase Signaling SystemLiver Cirrhosis, ExperimentalNetwork PharmacologyHepatic Stellate CellsRats, Sprague-DawleyPlant ExtractsDrug Therapy, CombinationLiver CirrhosisDisease Models, AnimalHumansMedicine, Tibetan TraditionalTransforming Growth Factor beta