Arctiin attenuates lipid accumulation, inflammation and oxidative stress in nonalcoholic fatty liver disease through inhibiting MAPK pathway

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease that predominantly affects the adult population. It was reported that arctiin improves functioning of the liver through multiple pathways, but the exact molecular mechanism is not clear yet. First, a mouse obesity model was successfully constructed, and hematoxylin and eosin staining and enzyme-linked-immunosorbent serologic assay (ELISA) were used to assess the levels of alanine aminotransferase and aspartate aminotransferase, respectively, in liver tissue damage. Then lipid accumulation in liver tissues was detected by immunohistochemistry (IHC) staining, and detection kits were used to determine the levels of triglycerides and total cholesterol in serum. Western blotting was used to detect the expression of adipose synthesis proteins, sterol regulatory element-binding protein-1, stearoyl-CoA desaturase-1 and fatty acid synthase, in liver tissues. Further, the levels of glutathione peroxidase, malondialdehyde, superoxide dismutase, catalase and reactive oxygen species as well as that of interleukin 2 (IL-2), IL-1β, IL-6 and tumor necrosis factor-α, and the expression of p-P65 and P65, in liver tissues were measured by ELISA and IHC, respectively. Finally, the protein expression levels of extracellular signal-regulated kinase (ERK), phospho-ERK, Jun N-terminal kinase, phospho-JNK, p38 and phospho-p38 in liver tissues were examined by WB. The results showed that relative to normal diet, mice on high-fat diet had increased body weight as well as fat content in liver tissues, increased liver tissue damage, decreased oxidative stress capacity and enhanced inflammatory response, while arctiin changed these adverse effects and inhibited mitogen-activated protein kinase (MAPK) pathway. Arctiin exerts hepatoprotective effects by inhibiting MAPK pathway and improving lipid accumulation, inflammatory response and oxidative stress.