https://www.selleckchem.com/products/4egi-1.html
GA also reduced neuronal loss and microglial activation. Cerebral Myd88 level showed a positive correlation with neurological scores. GA suppressed the expression of Myd88 and a proinflammatory pathway that included Myd88, HMGB1, TLR4, and NF-kappaB, as well as reducing serum concentrations of IL-1ß, IL-6, and TNF-alpha. CONCLUSIONS Post-treatment inhibited inflammatory responses and provided therapeutic benefits in diabetic mice with cerebral I/R injury, suggesting that GA may be a candidate drug to suppress cerebral I/R in diabetic pat