Schisandrol B

Schisandrol B (Gomisin-A) is a major active constituent of Schisandra chinensis with hepato-protective effects. Schisandrol B inhibits reactive oxygen species (ROS) production. Schisandrol B inhibits the activity of P-glycoprotein and CYP3A and also has anti-inflammatory, anti-diabetic and antioxidant activities^[1][2][3]. In Vitro: Schisandrol B (Gomisin-A; 1-10 μM; 2 days) treatment decreases the aging related inflammatory molecules, such as, COX-2, IL1β, and TNF-α. Schisandrol B attenuates the activity of senescence-associated β-galactosidase^[2].
Schisandrol B (Gomisin-A; 1-10 μM; 2 days) inhibits reactive oxygen species production even in the stress-induced premature senescence (SIPS)-human diploid fibroblast (HDF) cells^[2].
Schisandrol B (Gomisin-A; 1-10 μM) inhibits the MAPK pathway and the translocation of NF-κB to the nucleus^[2].
Schisandrol B (Gomisin-A; 1-10 μM) promotes the autophagy and mitochondrial biogenesis factors through the translocation of Nrf-2, and inhibits aging progression in the SIPS-HDF cells^[2].
Schisandrol B (0-80?μM) dramatically alters APAP metabolic activation by inhibiting the activities of CYP2E1 and CYP3A11^[1]. In Vivo: Schisandrol B (12.5?-200?mg/kg; oral administration; seven times with an interval of 12?hours) pretreatment significantly attenuates the increases in alanine aminotransferase and aspartate aminotransferase activity, and prevents elevated hepatic malondialdehyde formation and the depletion of GSH in a dose-dependent manner. Schisandrol B abrogates APAP-induced activation of p53 and p21, and increases expression of liver regeneration and antiapoptotic-related proteins such as cyclin D1 (CCND1), PCNA, and BCL-2^[1].