Background and Aim: Hepatic inflammation in nonalcoholic fatty liver disease (NAFLD) plays a pivotal role in the activation of the toll-like receptor-4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway, which is associated with the secretion of proinflammatory cytokines, exacerbation of oxidative stress, and induction of apoptosis. The first line of treatment for NAFLD is lifestyle intervention, including diet and exercise. Therefore, aim of this study was to investigate the combined effect of interval tarining with mealworm supplementation on the hepatic expression of inflammatory genes TLR4 and NF-κB and structural damage of liver tissue in rats with NAFLD. Materials and Methods: 25 rats, including five rats per group, were divided into five groups: healthy control, NAFLD model, model+exercise, model+supplement, and model+exercise+supplement. NAFLD modeling was performed with high-fat, cholesterol, and cholic-acid diet. The interval aerobic training was performed for eight weeks, five sessions per week at intensity of 50 to 80% of maximum running speed, for total of 30 minutes with overload; gavage of mealworm extract supplement was performed at dose of 20 mg/kg bodyweight. Hepatic expression of TLR4 and NF-κB genes was measured by Real-Time-PCR, accumulation of fat droplets in liver, sinusoidal expansion, and percentage of apoptosis by hematoxylin-eosin tissue staining. Data were analyzed by one-way ANOVA and Tukey's post-hoc tests at p≤0.05. Results: Induction of NAFLD led to increase in hepatic expression of TLR4 and NF-κB, accumulation of fat droplets, sinusoidal expansion, and percentage of apoptosis in liver tissue. Aerobic training, mealworm supplementation, and the combination of both interventions reduced the levels of all study indicators compared to NAFLD model group (p≤0.001). The combination of exercise and supplementation was able to restore TLR4 (98.7%) and NF-κB (97.6%) expression to healthy baseline compared to each of the independent interventions. Conclusion: The combination of aerobic training and mealworm, by creating positive changes in TLR4/NF-κB hepatic inflammation axis and modulating lipid metabolism, maybe more effective in treatment of NAFLD than either of the independent interventions.