BACKGROUND/

objectivesA high-fat diet (HFD) not only induces metabolic disorders but also causes oxidative damage to the lung tissue, triggering inflammatory responses. However, the detailed mechanisms by which HFD induces pulmonary oxidative stress and inflammation, particularly involving NF-κB/PPAR-γ signaling and lung microbiota, remain poorly understood, and effective dietary intervention strategies are still lacking. This study investigated the effects of HFD on lung tissue injury in mice and systematically evaluated the protective effects and potential mechanisms of

methodsAfter 12 weeks of HFD feeding, HFD group mice exhibited a marked increase in body weight (90.36%) compared with the control group, whereas body weight gain was significantly attenuated in the TGO (57.95%) and TGO-DG (55.78%) groups.

resultsBiochemical analyses revealed that the levels of malondialdehyde (MDA), nitric oxide (NO), and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) were significantly elevated in the HFD group, indicating pronounced oxidative stress and inflammatory responses in lung tissue. These symptoms were significantly attenuated by TGO and TGO-DG, with TGO-DG showing a more marked effect. Western blot (WB) results showed that both TGO and TGO-DG suppressed IL-6 expression and altered the expression of proteins in the NF-κB and PPAR-γ signaling pathways, which may contribute to the alleviation of pulmonary inflammation. Lung microbiota analysis revealed that TGO was associated with an increased proportion of

conclusionsOverall, these results suggest that TGO and TGO-DG effectively alleviate HFD-induced oxidative stress and inflammation in lung tissue through regulation of inflammatory signaling pathways and lung microbiota composition. Notably, TGO-DG exhibited superior protective effects, highlighting its potential as a lipid ingredient.