Schisantherin B

Schisantherin B (Gomisin-B) is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression^[1][2][3]. In Vitro:Schisantherin B (25 μM; 4 h) increases viability, inhibits apoptosis, and activates the PI3K/AKT pathway in H₂O₂-treated PC12 cells^[2]. In Vivo:Schisantherin B (15 mg/kg; i.p.; once daily for 10 consecutive days) exerts antidepressant-like effects in mice with depression induced by the forced swim test (FST), ameliorates FST-induced short-term memory impairment, and restores the activities of hippocampal GLT-1 and the PI3K/AKT/mTOR pathway^[1].
Schisantherin B (15 mg/kg; intravenous injection; three times daily) improves motor function, alleviates tissue damage, inhibits apoptosis and inflammatory responses, and activates the PI3K/AKT pathway to mitigate secondary injury, thereby promoting recovery in a mouse model of spinal cord injury^[2].
Schisantherin B (0.015-0.15 mg/kg; intracerebroventricular injection; once daily for 5 consecutive days) dose-dependently ameliorates Aβ_1-42-induced cognitive decline and neuronal damage in mice by restoring the functions of GLT-1 and GSK3β and reducing excessive tau phosphorylation^[3].
Schisantherin B (0.15 mg/kg; intracerebroventricular injection, once daily for 5 consecutive days) enhances spatial learning ability in healthy mice without altering their basal motor activity or inducing neuronal or biochemical abnormalities^[3].