Bioinformatic and chemoinformatic insights into mRNA and lncRNA dysregulation in metabolically associated fatty liver disease: the role of exercise and antioxidants following air pollution exposure

A common factor across chronic liver diseases is oxidative stress, which exacerbates disease pathology irrespective of the underlying causes. Exercise training (ET) and antioxidant-enriched supplements (AES) have emerged as recognized strategies for managing and preventing metabolic disorders, including those affecting liver health. This study conducted an <i>in silico analysis to identify switchable hub genes implicated in environmentally driven fatty liver disease, which were subsequently validated by</i> qPCR. Notably, dysregulation of key genes, including Il1-β, Fabp1, PPAR-γ, Cpt2, and Lxr, was observed in the air pollution (APE) group. Both ET and AES demonstrated regulatory effects on gene expression profiles before and after APE. Furthermore, our findings indicated that the expression levels of long non-coding RNAs (lncRNAs) Neat1 and H19 were significantly enhanced in the APE group. Notably, both ET and AES were shown to modulate the expression levels of these lncRNAs, further supporting the therapeutic potential of these interventions. Overall, our results suggest that APE alters the expression of mRNAs and lncRNAs, contributing to increased inflammation and metabolic disorders, while ET and AES offer promising strategies for the management and prevention of environmentally driven fatty liver disease.