Gomisin A

Gomisin A may exert neuroprotective effects by attenuating the microglia-mediated neuroinflammatory response via inhibiting the TLR4-mediated NF-κB and MAPKs signaling pathways. Gomisin A has anti-inflammatory property, potentially result from the inhibition of COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation. Gomisin A induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway. Gomisin A significantly inhibits cell proliferation in a dose-dependent manner, due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation. (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.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.Schisandrol B (Gomisin-A; 1-10 μM) inhibits the MAPK pathway and the translocation of NF-κB to the nucleus.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.Schisandrol B (0-80 μM) dramatically alters APAP metabolic activation by inhibiting the activities of CYP2E1 and CYP3A11.\n(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.