Fig. 1.
IL-1β and anoxia rapidly induce brainstem mPGES-1. mPGES-1 activity in the microsomal fraction of cortex and brainstem, including endothelial cells of the BBB, was analyzed in 9-d-old mice (n = 33) treated with IL-1β or vehicle and subjected to normoxia or normoxia plus anoxia (100% N2, 5 min). (A) In wild-type mice, mPGES-1 activity was measured at 90 min after NaCl (control) or 90 min and 180 min after IL-1β treatment. Higher endogenous mPGES-1 activity was observed in the brainstem compared with cortex in control mPGES-1+/+ mice. In addition, IL-1β induced mPGES-1 activity in a time-dependent manner. (B) At 90 min, IL-1β-treated mice exhibited approximately 2-fold higher activity in the brainstem compared with saline-treated mice. Anoxia also significantly induced mPGES-1 activity. Moreover, the effects of IL-1β and transient anoxic exposure were additive. When IL-1β-treated mice were exposed to anoxia, 4-fold higher activity was observed in the brainstem compared with control mice. However, mice with genetic deletion of mPGES-1 gene displayed negligible activity in response to IL-1β and anoxia. Data are presented as mean ± SEM. ∗, P < 0.05; ∗∗, P < 0.01; ∗∗∗, P < 0.001.