Protective Effect of Luteolin Isolated from Taraxacum coreanum Against Neuroinflammatory Responses Induced by Lipopolysaccharide: Involvement of Gut-Brain Axis.

Luteolin (LT) effectively lowered brain levels of pro-inflammatory mediators and cytokines triggered by LPS stimulation in mice.

• LT was administered at doses of 10 and 20 mg/kg/day
• Neuroinflammation was induced via lipopolysaccharide (LPS) injection in mice
• Both doses of LT reduced pro-inflammatory mediators and cytokines in brain tissue
• LT was isolated from Taraxacum coreanum, which is described as rich in luteolin

LT markedly elevated expression of tight junction proteins occludin and ZO-1 in the brain relative to LPS-treated mice.

• Occludin and ZO-1 are two tight junction proteins involved in blood-brain barrier integrity
• LPS-induced downregulation of these proteins was reversed by LT treatment
• Both 10 and 20 mg/kg/day doses of LT were assessed
• Upregulation of these proteins suggests maintenance of blood-brain barrier integrity

LT attenuated intestinal inflammatory mediator levels and markedly upregulated tight junction protein expression in the gut of LPS-injected mice.

• LT treatment reduced levels of inflammatory mediators in the intestine
• Tight junction protein expression in the intestine was markedly upregulated relative to the LPS-treated group
• These findings suggest LT protects gut barrier function in addition to the blood-brain barrier
• Gut barrier dysfunction is implicated in neuroinflammation via the gut-brain axis

LT markedly reversed LPS-induced gut microbiota dysbiosis by increasing the abundance of beneficial microbial taxa.

• Beneficial taxa increased by LT included Bacteroidota, Actinobacteriota, Murivaculaceae, and Lactobacillus
• LT reduced the relative abundance of Firmicutes and Desulfovibrio
• Desulfovibrio is among the taxa reduced, which is associated with gut inflammation
• These microbiota changes were observed relative to the LPS-treated group

The study investigated a gut-brain axis mechanism by which intestinal inflammatory agents and gut microbiota metabolites crossing the blood-brain barrier contribute to neuroinflammation.

• The research framework posits that intestinal inflammatory agents and metabolites generated by the gut microbiota can pass across the blood-brain barrier to induce neuroinflammation
• LPS was used as the inflammatory agent administered to mice to model this pathway
• LT's effects were assessed simultaneously in both the brain and gut compartments
• The study design examined tight junction integrity in both the gut barrier and blood-brain barrier