Schisanhenol

Schisanhenol (Schizanhenol), a lignan, is an orally active antioxidant. Schisanhenol reduces AChE activity, increases SIRT1 and PGC-1α expression, and decreases phosphorylated Tau (Ser 396) levels. Schisanhenol increases SOD and glutathione peroxidase activity, decreases malondialdehyde (MDA) content, and inhibits UGT2B7 activitY. Schisanhenol attenuates ox-LDL-induced apoptosis, intracellular reactive oxygen species generation, and cytotoxicity in endothelial cells. Schisanhenol inhibits LDL oxidation, brain mitochondrial and membrane peroxidative damage, and brain mitochondrial swelling and disintegration. Schisanhenol can be used for the research of Alzheimer’s disease, atherosclerosis, brain ischemia, and age-related brain deterioration^[1][2][3][4]. In Vitro:Schisanhenol attenuates ox-LDL-induced apoptosis and reactive oxygen species generation in cultured bovine aorta endothelial cells^[1].
Schisanhenol scavenges oxygen radicals in cultured human neutrophils^[1].
Schisanhenol protects cultured mouse spleen lymphocytes, isolated rat cerebral mitochondria and synaptosomes from oxygen free radical-induced injury^[1].
Schisanhenol (10-50 μM; 1 h pre-incubation, then 24 h co-incubation with ox-LDL) protects bovine aorta endothelial cells against ox-LDL-induced cytotoxicity in a dose-dependent manner, with 50 μM producing the strongest effect by preserving cell morphology, increasing cell viability, and reducing LDH leakage^[3].
Schisanhenol (10-50 μM; 24 h co-incubation with ox-LDL) inhibits ox-LDL-induced apoptosis in bovine aorta endothelial cells in a dose-dependent manner, with 10 μM producing a stronger reduction in sub-G1 apoptotic cells^[3].
Schisanhenol (10-50 μM; 30 min pre-incubation with DCFH-DA, then 15 min stimulation with ox-LDL) inhibits ox-LDL-induced intracellular reactive oxygen species generation in bovine aorta endothelial cells, with 10 μM returning ROS levels to normal control values^[3].
Schisanhenol (1-100 μM; 30 min) inhibits Fe²⁺-cysteine-induced lipid peroxidation and ATPase activity loss in 8-month-old rat brain membrane fractions in vitro in a dose-dependent manner^[4]. In Vivo:Schisanhenol (10-100 mg/kg; i.p.; daily; 7 days) attenuates Scopolamine (HY-N0296)-induced cognitive impairment, reduces hippocampal AChE activity and oxidative damage, and modulates the SIRT1-PGC-1α-Tau signaling pathway in male Kunming mice^[1].
Schisanhenol (150 mg/kg; p.o.) significantly increases brain cytosol glutathione-peroxidase activity in mice subjected to brain ischemia-reperfusion, with a measured activity of 0.898 nmol/mg/5 min^[4].