Artemisia absinthium attenuates hepatic fibrosis in mice by suppressing hepatic stellate cells activation and modulating inflammatory chemokine signaling.

Hepatic fibrosis is a chronic and progressive liver disease that can lead to cirrhosis or hepatocellular carcinoma. It represents a potentially reversible stage of chronic liver disease before progression to irreversible cirrhosis. Liver diseases can be effectively treated by inhibiting the fibrosis process. Artemisia absinthium is a medicinal plant traditionally used for liver illnesses. In the current study, mice were given 1.5 mL/kg CCl4 three times a week for two months in order to chemically induce liver fibrosis. A. absinthium 400 mg/kg methanol extract was assessed and contrasted with 100 mg/kg silymarin. The serum levels of AST, ALT, ALP and total bilirubin were assessed. Histopathological analysis revealed collagen buildup, necrosis, and injured hepatocytes in the CCl4 group. Artemisia absinthium suppressed the activation of hepatic stellate cells (HSCs) by downregulating the expression of TGF-β and PDGF-D and ultimately the expression of fibrotic and inflammatory markers including COL1A1, COL3A1, αSMA, Fn, Vim, Timp-2, IL-17 and TNF-α, via the TGF-β mediated SMAD, NF- κB and MAPK pathways. Artemisia absinthium limited the infiltration of monocytes in kupffer cells by downregulating the expression of chemokines (CCL2, CCL7) and associated cytokines (IL-17, TNF α), while upregulating the antifibrotic genes CX3CL1 and MMP2. In conclusion, the Artemisia absinthium extract attenuated liver fibrosis by inhibiting the activation of HSCs, kupffer cells and regulate the expression of related chemokines, cytokines, pro-inflammatory and pro-fibrotic markers.