Additional evidence supporting the above conclusion came from the observation that Claudin 5 protein expression was significantly restored, and a subsequent decrease in proinflammatory cytokines IL-6 and IL-1β secretion was observed in 24p3RsiRNA (a blocked Lcn2 receptor) exposed brain endothelial cells that were co-incubated with Lcn2 or serum of NASH mice. Here, CLDN5 is linked to metabolic dysfunction-associated steatohepatitis.