Study on mitigating effect and mechanism of Cichorium glandulosum n-butanol extraction site on CCl₄-induced chronic liver injury in rats.

This study aims to investigate the mitigating effect and mechanism of Cichorium glandulosum n-butanol extraction site (CGE) on the disease in carbon tetrachloride (CCl₄) -induced chronic liver injury model in rats. A chronic liver injury model was constructed by subcutaneous injection of CCl₄ olive oil solution, and after four weeks of CGE treatment, serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), hydroxyproline (HYP), interleukin-4 (IL-4), interleukin-6 (IL-6), malondialdehyde (MDA), superoxide dismutase (SOD), and tumor necrosis factor-α (TNF-α) were detected. Liver tissue was processed by hematoxylin-eosin (HE) staining and Masson staining to observe the structure of the rat liver. qPCR and Western blot were used to examine the expression of transforming growth factor-β1 (TGF-β1) /small mothers against decapentaplegic (Smad), Toll-like receptor 4 (TLR4), α-smooth muscle actin (α-SMA), and fibronectin (Fn) in rat liver tissue and hepatic stellate-T6 (HSC-T6) and evaluate the inhibitory effect of CGE on HSC activation. The results showed that CGE could significantly reduce the serum levels of AST, ALT, AKP, HYP, and affect the levels of related inflammatory indexes including IL-4, IL-6, and TNF-α, and MDA in CCl₄-induced chronic liver injury in rats and had no effect on SOD activity, which could delay the process of liver injury, alleviate the hepatic collagen deposition and inflammatory infiltration, and had significant efficacy in mitigating chronic liver injury in rats. CGE could inhibit α-SMA and TLR4 protein expression in the liver tissue and reverse the increased TGF-β1/Smad, Fn, and TLR4-related expression in HSC-T6 in vitro. The above results indicated that CGE exerted hepatoprotective effects in rats by inhibiting HSC activation and alleviated CCl₄-induced chronic liver injury in rats and could ameliorate inflammatory response and slight liver fibrosis in rat liver tissue. Its pharmacodynamic mechanism might be related to TGF-β1/Smad and TLR4-related expression.