Salvianolic acid C (20 mg/kg) treatment could significantly decrease the escape latency. In addition, SalC (10 and 20 mg/kg) treatment significantly increase the platform crossing number compared with the LPS model group. Systemic administration of Salvianolic acid C down regulates the brain TNF-α, IL-1β and IL-6 levels compared with the model group. The iNOS and COX-2 levels in rat brain cortex and hippocampus are higher than that in the control group, while Salvianolic acid C treatment significantly down regulates the cortex and hippocampus regions. Salvianolic acid C (5, 10 and 20 mg/kg) treatment dose-dependently increases the p-AMPK, Nrf2, HO-1 and NQO1 levels in rat brain cortex and hippocampus[2].
