Objective:To explore any effect of regular aerobic exercise on liver fibrosis in rats with non-alcoholic fatty liver disease (NAFLD) and its mechanism.Methods:Twenty-four 8-week-old male OLETF rats were randomly divided into a model sedentary group and a model exercise group, each of 12. Twelve age- and sex-matched LETO rats of the same strain were selected into the healthy control group. The model exercise group underwent treadmill exercise training for 12 weeks, while the other two groups undertook no exercise. After the training, fasting blood glucose, insulin and glycosylated hemoglobin (HbA1c) were measured using colorimetry. Liver tissue was resected to observe any histopathological changes using Masson staining and to measure the collagen volume fraction. Zymography was applied to determine the activities of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the liver. Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), α-smooth muscle actin (αSMA), cysteine-rich protein 61 (CCN1), transforming growth factor-β (TGF-β), MMP-12 and the tissue inhibitor of metalloproteinase-1 (TIMP-1) proteins in the liver were quantified using western blotting.Results:Compared with the healthy control group, the model sedentary group on average displayed a significant increase in body weight, fasting blood glucose, fasting insulin, HbA1c, liver collagen volume fraction, and the protein expression of TGF-β, αSMA, CCN1, IL-1β, TNF-α, and MMP-12. There was a significant decrease in the activity of MMP-2 and MMP-9 on average. Compared with the model sedentary group, the model exercise group on average displayed lower fasting blood glucose, fasting insulin, HbA1c, and liver collagen volume fraction, as well as less expression of TGF-β, αSMA, IL-1β, TNF-α, and MMP-12 protein. MMP-2 and MMP-9 activity was higher, as was the expression of CCN1 protein. There were no significant differences in average body weight between the model sedentary and exercise groups.Conclusion:Regular exercise can delay liver fibrosis, at least in NAFLD rats. The mechanism is related to inhibiting hepatic inflammatory response, the activation of hepatic stellate cells and improving extracellular matrix remodeling.