Abstract: AIM: To investigate the protective effect of ligustrazine on fatty liver induced by carbon tetrachloride in mice and study the possible mechanisms. METHODS: The fatty liver model was established by 0.5 % carbon tetrachloride (CCl4)-oil solution i. p. on the first day of the experiment. One hour before the model was made, mice in high-dose, middle-dose and low-dose groups were given ligustrazine 50, 25 and 12.5 mg/kg i.p., respectively. Furthermore, the model group, Tiopronin group and different dosages of ligustrazine groups were taken normal saline, Tiopronin 200 mg/kg, and ligustrazine 50,25 and 12.5 mg/kg i.p., respectively, twice a day for 7 days. The indexes of liver function such as levels of GOT and GPT in serum were evaluated. The liver lipid and lipid superoxidation were measured, and pathology was examined. RESULTS: Compared with the model group, the activities of ALT and AST significantly decreased in serum (P<0.05) ;Ligustrazine markedly decreased the contents of triglycerides (TG) (P<0.05) and free fatty acid (FFA) (P<0.01) in liver tissue ;the activities of lipase and SOD were higher (P<0.05) , and the content of malondialdehyde (MDA ) decreased markedly (P<0.05 or P<0.01) in liver tissue. CONCLUSION: Ligustrazine improves the protective effect on injury liver in mice and decreases the deposition of triglycerides in liver. The possible mechanism is that ligustrazine can reduce the TG deposition, promote the β-oxidation of FFA and decrease the lipid peroxidation injury.

Key words: ligustrazine, fatty liver, lipid, free fatty Acid