The effects and mechanism of Aronia melanocarpa Elliot anthocyanins on hepatic fibrosis

Highlights

• Studies have shown that AMA has anti-fibrotic effects on CCl4-induced liver injury in mice.

• AMA treats hepatic fibrosis by inhibiting the TGF-β signaling pathway.

• AMA inhibits hepatic fibrosis by reducing the expression of inflammatory factors such as TNF-α and IL-1.

Abstract

Hepatic fibrosis is a pathological change that is a major problem in chronic liver disease. As an important biologically active substance, the Aronia melanocarpa Elliot anthocyanins (AMA) has a strong anti-oxidation property and may have certain preventive and therapeutic effects on hepatic fibrosis diseases. The current research was designed for evaluation the antifibrotic effects and mechanism of AMA on CCl₄-induced liver injury in mice. Mice injected with CCl₄ twice a week at the same time as treated with 20 or 40 mg/kg AMA by gavage every day. After 8 weeks, biochemical parameters were used to estimate liver damage, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total serum bilirubin (TSB), total protein (TP) and albumin (ALB). In addition, oxidative stress parameters such as superoxide dismutase (SOD) and reduced glutathione (GSH) were also studied. And the role of TNF-α, IL-1, IL-6, COX-2 as markers of inflammation at the transcriptional level. Histopathological examination of liver tissue was performed and compared to controls. Collagen I, alpha smooth muscle actin (α-SMA), transforming growth factorβ1 (TGF-β1) and SMAD2 were also evaluated as markers of fibrosis. The results showed that AMA improved CCl₄-induced fibrosis, such as histopathological scores, markers of liver damage and oxidative stress. In addition, we investigated the potential mechanisms of underlying these effects, including: (1) inhibiting fibrosis by reducing the expression of inflammatory factors such as TNF-α and IL-1; (2) Prevent liver fibrosis by inactivating α-SMA expression; (3) inhibition of TGF-β1 secretion and Collagen I deposition to down-regulate the fiber reaction of HSC. In conclusion, this study illustrated the anti-fibrotic effects of AMA and may be a new candidate for the treatment of hepatic fibrosis.