Baicalein improves sepsis-associated encephalopathy via suppressing oxidative stress and iNOS-mediated NO production and enhancing BDNF/TrkB signaling

Baicalein is a medicinal herb and has various biological activities. Our present work aimed to evaluate the protective effect of baicalein on sepsis-associated encephalopathy (SAE) and further probe the potential mechanisms. SAE model was prepared using cecal ligation and puncture in mice. Animals were treated with saline or baicalein by doses of 10, 20 and 40 mg/kg for seven consecutive days. Neuronal function was assessed with the Open Field tests, Morris Water Maze task and Y Maze tests. The serum ammonia levels were measured after SAE. Besides, malondialdehyde (MDA) contents and the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and inducible nitric oxide synthase (iNOS) activities were also detected using respective commercial kits. Detection of NO production was conducted using Griess reagent. No significance was found in Open Field test. However, the cognitive deficits were remarkably improved in SAE-induced mice after baicalein treatment based on the results of Morris Water Maze and Y Maze tests. Meanwhile, baicalein didn't alter the serum ammonia levels in SAE-induced mice. But baicalein significantly suppressed oxidative stress, the protein levels of iNOS and NO production while the protein expressions of BDNF was found to be markedly enhanced in mice with SAE after baicalein treatment. It was concluded that baicalein reversed cognitive deficits in a mouse model of SAE via suppressing oxidative stress and iNOS-mediated NO production and activating BDNF/TrkB signaling.