Fig. 7.

Effects of EETs increased by sEH inhibition with AUDA on the main components of molecular mechanism of fever. On the diagram, ↓ arrowheads represent activation while ⊥ inhibition. As a result of AUDA administration in the course of febrile response to inflammatory stimuli, DHET formation is inhibited and EETs produced from arachidonic acid by cytochrome P-450 monooxygenase are increased and available for a prolonged period. EETs acting by the mechanisms described in the discussion section lead to downregulation in fever mediators—cytokines and prostaglandins—thereby weakening fever