Salvianolic acid C is a noncompetitive Cytochrome P4502C8 (CYP2C8) inhibitor and a moderate mixed inhibitor of Cytochrome P45022J2 (CYP2J2), with K_is of 4.82 μM and 5.75 μM for CYP2C8 and CYP2J2, respectively. IC50 & Target: Ki: 4.82 μM (CYP2C8), 5.75 μM (CYP2J2)^[1]. In Vitro: Salvianolic acid C is a noncompetitive CYP2C8 inhibitor and a moderate mixed inhibitor of CYP2J2, with K_is of 4.82, 5.75 μM for CYP2C8 and CYP2J2, respectively^[1]. 1 and 5 μM Salvianolic acid C (SalC) could significantly inhibit the NO production induced by LPS. Salvianolic acid C decreases the expression of iNOS significantly. Salvianolic acid C inhibits LPS-induced TNF-α, IL-1β, IL-6 and IL-10 overproduction. Salvianolic acid C inhibits LPS-induced NF‑κB activation. Salvianolic acid C also increases the expression of Nrf2 and HO-1 in BV2 microglial cells^[2]. In Vivo: 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].