Cox-1/Cox-2 Inhibition on Expression of Glial Aromatase Following Traumatic Brain Injury in Mice (Mus musculus)
Tony Joo, Vassar College ’16 and Prof. Kelli DuncanFollowing brain injury, the upregulation of glial aromatase induces the synthesis of neutrally derived estrogens. These estrogens inhibit neurodegeneration and neuroinflammation while promoting repair and recovery in the vertebrate brain. Although it is clear that estrogens are neuroprotective, the specific pathway mediating this process remains unknown. Prostaglandin E2 (PGE2) has been shown to regulate aromatase expression and is formed from the conversion of arachidonic acid to prostaglandin via the Cyclooxygenase (Cox-1 and Cox-2) enzymes. Cox-1 is constitutively expressed and provides homeostatic regulation of prostaglandin levels, whereas Cox-2 is inducible and promotes neuroinflammation. The goal of this experiment was to determine if either Cox-1 or Cox-2 regulate the induction of glial aromatase following injury. Bilateral cannulas were implanted into the hippocampus of both male and female adult wild-type mice (Mus musculus). After injury, mice were treated with either Naproxen (Cox-1 selective non-steroid anti-inflammatory (NSAID)), Celecoxib (Cox-2 selective NSAID), or vehicle (peanut butter) for 7 days. Eight days post-surgery, brain tissue was collected for aromatase analysis, and trunk blood was collected for cytokine and prostaglandin expression (IL-1β, IL-6, TNF α, PGE2).