Despite many recent studies on non-alc. fatty liver disease (NAFLD) therapeutics, the optimal treatment has yet to be determinedIn this unfinished project, we combined secondary metabolites (SMs) from the gut microbiota (GM) and Hordeum vulgare (HV) to investigate their combinatorial effects via network pharmacol. (NP).Addnl., we analyzed GM or barley - signalling pathways - targets - metabolites (GBSTMs) in combinatorial perspectives (HV, and GM).A total of 31 key targets were analyzed via a protein-protein interaction (PPI) network, and JUN was identified as the uppermost target in NAFLD.On a bubble plot, we revealed that apelin signalling pathway, which had the lowest enrichment factor antagonize NAFLD.Holistically, we scrutinized GBSTM to identify key components (GM, signalling pathways, targets, and metabolites) associated with the Apelin signalling pathway.Consequently, we found that the primary GMs (Eubacterium limosum, Eggerthella sp. SDG-2, Alistipes indistinctus YIT 12060, Odoribacter laneus YIT 12061, Paraprevotella clara YIT 11840, Paraprevotella xylaniphila YIT 11841) to ameliorate NAFLD.The mol. docking test (MDT) suggested that tryptanthrin-JUN is an agonist, conversely, dihydroglycitein-HDAC5, 1,3-diphenylpropan-2-ol-NOS1, and (10[(Acetyloxy)methyl]-9-anthryl)methyl acetate-NOS2, which are antagonistic conformers in the apelin signalling pathway.Overall, these results suggest that combination therapy could be an effective strategy for treating NAFLD.