[Abstract] Objective: To study the inhibitory effect of Huaganjiedu decoction on liver fibrosis in rats with chronic hepatitis B by regulating TLR4 signaling pathway. Methods: 50 SPF SD rats were randomly selected to establish the rat liver fibrosis model by intraperitoneal injection of carbon tetrachloride (CCl4), and the remaining 10 rats were recorded as blank control group and injected with equal volume of normal saline. The rats successfully modeled were randomly divided into 5 groups: Huaganjiedu decoction high, medium, and low dose groups, silibinin group and model group. Huaganjiedu decoction high, medium, and low dose groups were given 9.2 g/kg, 4.6 g/kg, and 2.3 g/kg Huaganjiedu decoction. Silibinin group was given 50 mg/kg silibinin. The blank control group and the model group were given the same volume of normal saline. Once a day for 8 weeks. After treatment, Toll-like receptor 4 (TLR4), transcription factor NF-κB (NF-κB), transforming growth factor-β1 (TGF-β1), hyaluronic acid (HA), laminin (LN) content were detected by enzyme-linked immunosorbent assay (ELISA), The pathological changes of rat liver were observed by hematoxylin eosin (HE) staining. The liver fibrosis of rats was observed by Masson staining. Detection of TLR4, MyD88, NF-κB, TGF-β1 mRNA expression in rat liver tissue by fluorescence quantitative polymerase chain reaction (RT-qPCR). Detection of TLR4, MyD88, total NF-κB, nuclear NF-κB, cytoplasmic NF-κB, TGF-β1 protein expression levels in rat liver tissue by Western blot (WB). Results: Serum TLR4, NF-κB, TGF-β1, HA, LN levels in the model group were higher than the blank control group (P<0.05), and the silibinin group and the Huaganjiedu decoction high, medium and low dose groups were lower than the model group (P < 0.05). The liver lobule structure of the model group were destroyed, the liver lobule were replaced by the pseudolobule, and a large amount of inflammatory cell infiltration and a large amount of collagen fiber hyperplasia appeared in the liver tissues. Compared with the model group, the Huaganjiedu decoction high, medium and low dose groups and silibinin group showed improvement, and the Huaganjiedu decoction high dose group was the closest to the blank control group. Rat liver tissue TLR4, MyD88, NF-κB, TGF-β1 mRNA and protein expression levels and nuclear NF-κB protein expression level in the model group were higher than that in the blank control group (P < 0.05), the silibinin group and Huaganjiedu decoction high, medium and low dose groups were lower than the model group (P < 0.05). Conclusion: Huaganjiedu decoction can improve serum liver fibrosis indexes, alleviate liver tissue lesions, and alleviate liver fibrosis. It is speculated that its mechanism may be related to the inhibition of TLR4 signaling, down-regulate the expression levels of TLR4, MyD88, NF-κB mRNA and protein, and inhibit NF-κB nuclear displacement, downstream TGF-β1 pathway inhibited thereby reducing serum HA and LN levels. |