Gomisin J

Gomisin J is a Schisandra chinensis-derived lignan that can inhibit multiple targets such as eNOS, AMPK (LKB1, CaMKIIβ), fetuin-A, NF-κB, Nrf2/HO-1, and can pass through the blood-brain barrier. Gomisin J increases NO bioavailability by activating eNOS, regulates lipid metabolism by activating the AMPK pathway, inhibits fetuin-A and NF-κB to exert anti-inflammatory effects, and activates Nrf2/HO-1 to enhance antioxidant capacity. Gomisin J has the activities of anti-hypertension, regulating liver lipid metabolism, and reducing cerebral ischemia-reperfusion injury, and can be used for research on hypertension, non-alcoholic fatty liver disease, cerebral ischemia-reperfusion injury, etc^[1][2][3]. In Vitro:Gomisin J (10-200 μM; 24 h) has no significant effect on HepG2 cell viability at low doses (≤50 μM)^[2].
Gomisin J (10-40 μM; 24 h) reduces lipid accumulation and TG content induced by oleic acid (HY-N1446) in HepG2 cells, downregulates lipogenic proteins (SREBP-1c, FAS), upregulates lipolytic proteins (PPARα, PGC-1α), activates AMPK and ACC phosphorylation^[2].
Gomisin J (10-40 μM; 24 h) downregulates lipogenic genes (SREBP-1c, FAS, etc.) and inflammatory genes (TNF-α, MCP-1, etc.) in HepG2 cells, upregulates lipolytic genes (PPARα, CPT-1, etc.), and has LKB1-dependent AMPK activation^[2].
In Vivo:Gomisin J (1 μg/kg/min and 3 μg/kg/min; osmotic minipump, subcutaneous injection; continuous administration; 14 days) reduces blood pressure, restores plasma NO metabolite levels and vascular NO production, and reduces vascular ROS generation in the Ang II-induced hypertension model of C57BL/6 mice^[1].
Gomisin J (5-80 mg/kg; intraperitoneal injection; single dose before reperfusion; observation until 48 h after reperfusion) dose-dependently reduces neurological function scores, cerebral infarct volume and brain water content, inhibits hippocampal neuronal apoptosis, and reduces inflammation and oxidative stress in the middle cerebral artery occlusion/reperfusion (MCAO/R) model of Wistar rats^[3].