Phytochemicals from lingonberry have rich pharmacological value and may play an essential role in treating
liver diseases. We investigated the regulatory role of lingonberry
anthocyanins (LA) on HSC activation in vitro and liver fibrogenesis in vivo. The viability of HSCs treated with LA was significantly reduced in a dose-dependent manner at the concentration of 25-100 μg/mL, in which the monomers of LA also reduced the proliferation of HSCs via IC50 assay. The inducer
transforming growth factor β1 (TGFβ1) and the effector α-smooth muscle actin (α-SMA) of HSC activation were all decreased both in
protein and
RNA levels treated by LA. Moreover, LA alleviated CCl4-induced
liver fibrosis in rats, reducing
collagen aggregation and production and decreasing the
hydroxyproline (HYP) and
malondialdehyde (MDA) levels in the liver tissue. Moreover, LA reduced the indexes of serum
liver fibrosis and reversed the index of serum liver function in CCl4-induced rats. Furthermore, the
antioxidant enzymes, including
superoxide dismutase (SOD),
glutathione peroxidase (GSH-Px), and
catalase (CAT), in the liver tissue and serum were significantly increased upon treatment with LA. Importantly, LA promoted hepatic parenchymal cell proliferation and inhibited the expression of TGFβ/Smad/extracellular regulated
protein kinase (ERK) signaling pathway-related genes. This study demonstrates the anti-
liver fibrosis activity of LA and investigates its mechanism, which may provide a novel strategy for treating
liver fibrosis using lingonberry.