Research Interests

• The pathogenesis of septic encephalopathy (SAE): 1. Increased expression of soluble surface oxide hydrolase (sEH) leads to decreased levels of epoxide fatty acid EETs in the brain, which is a key mechanism causing cognitive dysfunction of SAE. sEH is mainly expressed on endothelial cells in the nervous system, which is an important site of brain lipid metabolism and an important component of the blood-brain barrier. 2. Septic encephalopathy leads to changes in ubiquitin hydrolase UCH-L1 activity, which may play a significant role in long-term cognitive dysfunction in septic encephalopathy.