In conclusion, the above results represented that high circulatory Lcn2 in MAFLD/NASH induces blood-brain barrier disruption by altering expression of tight junction proteins Claudin 5, ZO1, and induced the secretion of proinflammatory cytokines IL-6 and IL-1β in brain endothelial cells. Here, LCN2 is linked to metabolic dysfunction-associated steatohepatitis.