Abstract
The present study aimed to assess the protective effects of tetramethylpyrazine (TMP) on the livers of mice fed a high fat diet. The mice were divided into five groups: Regular diet; high fat diet; simvastatin‑treated; and low and high dose TMP‑treated groups. The results demonstrated that, compared with the control group, serum glucose, total cholesterol (TC) and low‑density lipoprotein cholesterol levels were increased in the model group. Additionally, compared with the model group, simvastatin lowered the TC level, whereas TMP did not. Compared with the control group, the level of malondialdehyde (MDA) in the liver tissue was increased and the level of glutathione peroxidase (GSH‑pX) in the liver tissue was decreased in the model group. Furthermore, compared with the model group, TMP decreased the level of MDA and increased the level of GSH‑Px; however, simvastatin did not have these effects. Immunohistochemistry and western blotting were performed; the results showed that, compared with the control group, the levels of inflammatory factors (tumor necrosis factor‑α and interleukin‑6) in the liver tissue were increased, and the ratio of phosphorylated (p)‑nuclear factor κB (NF‑κB)/NF‑κB was also increased in the model group. The addition of TMP and simvastatin demonstrated that, compared with the model group, the inflammatory factor levels and the ratio of p‑NF‑κB/NF‑κB were decreased. In addition, liver lipid deposition was examined in the model group using hematoxylin and eosin staining and Oil Red O staining, and the results showed that TMP and simvastatin reduced liver lipid deposition. Furthermore, compared with the control group, the reactive oxygen species (ROS) level in the liver tissue was increased. Compared with that in the model group, TMP and simvastatin decreased the ROS level. In conclusion, TMP, similar to simvastatin, exerted a notable hepatoprotective effect on mice fed a high fat diet with non‑alcoholic fatty liver disease, by inhibiting inflammatory factors and the p‑NF‑κB/ROS signaling pathway.