Raspberry Ketone Attenuates LPS‐Induced Glial Inflammation and Lipid Droplet Accumulation

Neuroinflammation driven by glial activation and metabolic imbalance is implicated in neurological dysfunction. Raspberry ketone (RK), a food‐derived phenolic compound, remains poorly characterized in glial inflammatory regulation. Here, RK was evaluated in lipopolysaccharides (LPS)‐challenged mice and in glial cell models. RK reduced circulating cytokines and attenuated inflammatory responses in the cortex, hippocampus, and hypothalamus. In microglial and astrocytic models, RK suppressed LPS‐induced inflammatory activation without detectable cytotoxicity. Transcriptomic analysis showed that RK partially reversed the LPS‐induced inflammatory gene program, notably Tnf , NF‐κB , and cytokine–cytokine receptor interaction pathways, with Il6 , Il1b , and Tnf identified as hub genes. RK was associated with suppression of TLR4/NF‐κB signaling, accompanied by reduced p65 phosphorylation, and improved lipid homeostasis by decreasing lipid droplet accumulation and Plin2 expression. These findings highlight RK as a food‐derived bioactive that modulates glial inflammatory and lipid metabolic responses.