SLC27A3-dependent lipid metabolic reprogramming by trilobatin suppresses microglial mtDNA/TLR9-driven inflammatory activation in traumatic brain injury - PubMed
3 hours ago
- #neuroinflammation
- #lipid metabolism
- #trilobatin
- Trilobatin reduces neuroinflammation and improves motor and cognitive outcomes in a traumatic brain injury mouse model.
- Excessive fatty acid uptake post-TBI leads to lipid droplet accumulation, mitochondrial stress, and pro-inflammatory activation in microglia.
- Trilobatin downregulates lipid transporter SLC27A3, limiting lipid uptake and alleviating mitochondrial lipid accumulation and damage.
- Inhibition of mitochondrial DNA release by trilobatin blocks the TLR9/MyD88/P-P65 pro-inflammatory pathway.
- The study links microglial lipid metabolism to inflammatory activation, supporting trilobatin as a therapeutic agent for acute neural injury.