ArticleMolecular biology reports2026
Esculin attenuates cholestatic liver injury and fibrosis in bile duct-ligated rats by modulating oxidative stress, inflammatory responses, and fibrogenic mediators.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCholestatic liver injury is a major contributor to hepatic fibrosis and cirrhosis, yet effective pharmacological therapies remain unavailable. Esculin, a natural coumarin glucoside, possesses potent antioxidant and anti-inflammatory activities, but its potential to mitigate cholestasis-associated fibrosis has not been fully elucidated. This study aimed to evaluate the hepatoprotective and antifibrotic effects of esculin in bile duct ligation induced cholestatic rats.
methodsForty male Sprague-Dawley rats were divided into four groups: control, BDL, BDL + esculin 20 mg/kg, and BDL + esculin 40 mg/kg. Esculin was administered orally for 14 consecutive days starting on day 7 post-surgery. Serum biochemical markers, hepatic oxidative stress parameters, fibrogenic mediators (LOX, hydroxyproline, and glycosaminoglycans), and mRNA expression of IL-1β, TNF-α, NF-κB, and TGF-β1 were quantified. Histopathological and immunohistochemical analyses (α-SMA staining) were performed to assess tissue architecture and stellate cell activation.
resultsBDL-induced cholestasis caused marked hepatocellular injury, oxidative imbalance, inflammation, and fibrosis, as evidenced by elevated ALT, AST, ALP, bilirubin, MDA, LOX activity, and pro-fibrogenic gene expression. Esculin treatment significantly attenuated these alterations in a dose-dependent manner, restoring antioxidant defenses (SOD, GPx, TAC), reducing lipid and protein oxidation, and downregulating NF-κB/TGF-β1 signaling. Histological findings confirmed improved hepatic architecture, reduced collagen accumulation, and diminished α-SMA immunoreactivity.
conclusionThese findings suggest that esculin exerts hepatoprotective and antifibrotic effects through coordinated modulation of oxidative stress, inflammatory responses, and fibrogenic mediators, as evidenced by reduced NF-κB and TGF-β1 mRNA expression together with decreased LOX activity.
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