BACKGROUNDː Metabolic syndrome (SM) is a pathophysiological disorder that can cause chronic inflammation mediated by decreased levels of leptin and adiponectin that are unable to inhibit proinflammatory mediators, such as IL-6, TNF-α. In addition, PPAR (peroxisome proliferator activator receptor) γ, with its role in SM and pulmonary fibrosis, can inhibit inflammation. Objective: To analyze the effects of metabolic syndrome on lung fibrosis, IL-6, TNF-α, and PPARγ expression in lung tissue and serum of Sprague Dawley rats. METHODSː The study used a true experimental design, pre and post test control group on 20 male Sprague-Dawley rats aged 37 weeks, divided into 2 groups, namely control and metabolic syndrome. RESULTSː Plasma and tissue TNF-α levels in SM rats were higher than the control group (p=0.010, 0.000). The degree of fibrosis and the area of lung fibrosis in the SM group was higher than the control with (p=0.000). There was a correlation between TNF-α both plasma and tissue to the area of fibrosis with a correlation coefficient of 0.464 and 0.814 respectively (p = 0.039 and 0.000). There were significant correlations of increased body weight (0.977, p=0.00), fasting blood sugar (0.906, p=0.00), triglycerides (0.912, p=0.00) and decreased HDL (-0.903, p=0.00), with increased blood plasma IL-6 (0.873, p=0.00), lung tissue IL-6 (0.761, p=0.00), and the extent of lung tissue fibrosis (0.816, p=0.00). SM in the rat model was significantly inversely correlated with PPARγ expression in both plasma (Pearson: -0.867, p<0.05) and lung tissue (Pearson: -0.867, p<0.05), indicating decreased and increased PPARγ levels. CONCLUSIONSː Metabolic syndrome significantly correlates with lung damage in the form of increased plasma and tissue levels of IL-6 and TNF-α, as well as the degree of lung tissue fibrosis. Metabolic syndrome significantly decreased PPARγ expression in serum and tissue.