For research use only.
Storage
3 years,-20°C,powder
1 years,-80°C,in solvent
In vivo
Parecoxib, a selected cyclooxygenase-2 inhibitor, ameliorates neurologic deficits in the behavior studies and brain damage, including neuronal death, and brain edema in the MCP-1 and NeuN immunostaining in rats subjected to SAH(Subarachnoid Hemorrhage). Parecoxib is able to reduce early COX2 expression via inhibiting cJNK (p55) expression (dose-dependently), reduce IL-1β, IL-6 and MCP-1( at 2000 ug/kg/day at the time point of 24hr and 72hr after the induction of SAH), IL-8 (of the dosage of 2000 ug/kg/day at 24hr after the induction of SAH), and also reduce cleaved caspase-1 (at 1000 and 2000 ug/kg/day) and Caspase-9a (at 2000 ug/kg/day). Parecoxib reduces the NMDAR-1, and NMDAR-2a (at 1000 and 2000 ug/kg) after the induction of SAH.