5-O-Methylvisammioside

5-O-Methylvisammioside (4'-O-β-D-Glucosyl-5-O-methylvisamminol) is an orally active natural chromone glycoside and multiple biological activities. 5-O-Methylvisammioside inhibits ferroptosis by activating the Nrf2/HO-1 signaling axis. 5-O-Methylvisammioside alleviates intestinal barrier damage by inhibiting the ROS/NF-κB/NLRP3 pathway. 5-O-Methylvisammioside exerts a protective effect against acute liver injury by reducing ALT/AST, decreasing inflammatory infiltration, and inhibiting IκB-α phosphorylation and NF-κB nuclear translocation. 5-O-Methylvisammioside blocks the HMGB1/RAGE/MEK/ERK signaling axis to exert anti-tumor and anti-angiogenic effects. 5-O-Methylvisammioside improves depression-like behaviors by inhibiting Src kinase and the NF-κB pathway^{[1][2][3][4][5]}. In Vitro:5-O-Methylvisammioside effectively blocks the production of inflammatory cytokines induced by lipopolysaccharide in BV-2 microglial cells^[1].
5-O-Methylvisammioside (50-500 μg/mL; 24 h) shows no toxicity to human umbilical vein endothelial cells at concentrations up to 500 μg/mL, and inhibits HMGB1-induced proliferation of human umbilical vein endothelial cells in a dose-dependent manner^[2].
5-O-Methylvisammioside (100-500 μg/mL; 24 h) dose-dependently inhibits HMGB1-induced migration of human umbilical vein endothelial cells in wound healing assays^[2].
5-O-Methylvisammioside (100-500 μg/mL; 24 h) dose-dependently inhibits HMGB1-induced migration of human umbilical vein endothelial cells in Transwell assays^[2].
5-O-Methylvisammioside (100-500 μg/mL; 16 h) dose-dependently inhibits HMGB1-induced tube formation in human umbilical vein endothelial cells^[2].
5-O-Methylvisammioside (100-500 μg/mL) dose-dependently inhibits HMGB1-induced upregulation of RAGE, phosphorylated MEK, and phosphorylated ERK in human umbilical vein endothelial cells^[2].
5-O-Methylvisammioside (250 μg/mL) inhibits HMGB1-induced upregulation of RAGE in human umbilical vein endothelial cells^[2].
5-O-Methylvisammioside (100-500 μg/mL) dose-dependently inhibits HMGB1-induced VEGF production in human umbilical vein endothelial cells^[2].
5-O-Methylvisammioside (40 μM; 48 h) significantly reduces oxidative stress levels, corrects iron metabolism disorders, restores the expression levels of ferroptosis-related proteins, and decreases proinflammatory cytokine levels in Erastin (HY-15763)-treated Caco-2 cells. These protective effects strictly depend on the Nrf2/HO-1 pathway, as Nrf2 knockdown significantly attenuates the aforementioned effects^[3].
5-O-Methylvisammioside (10 μM; 45 min) potently inhibits CNT2-mediated adenosine uptake in HEK293 cells overexpressing CNT2, with an IC₅₀ of 11.22 μM, and exhibits stronger activity than other tested compounds at the concentration of 10 μM^[4].
5-O-Methylvisammioside (10 μM; 24 h) inhibits ROS production in human intestinal epithelial cells stimulated with 720 μM uric acid (UA) (HY-B2130) for 24 h, which is confirmed by reduced DCFH-DA fluorescence intensity and regulated mRNA expression of SOD/NOX4^[4].
5-O-Methylvisammioside (10 μM; 24 h) inhibits the activation of the ROS/NF-κB/NLRP3 pathway and restores the expression of tight junction proteins in human intestinal epithelial cells stimulated with 720 μM UA for 24 h^[4]. In Vivo:5-O-methylvisammioside (5-10 mg/kg; i.p.; once daily; 7 days) ameliorates Acetaminophen (HY-66005)-induced acute liver injury in male ICR mice by inhibiting the TNF, MAPK, NF-κB, and arachidonic acid pathways, reducing serum liver enzyme and inflammatory cytokine levels, and improving liver histopathology^[1].
5-O-Methylvisammioside (12.5-50 mg/kg; once daily; 14 days) dose-dependently inhibits orthotopic hepatocellular carcinoma growth in C57BL/6 mice, with a maximum tumor inhibition rate of 62.64% at 50 mg/kg, by suppressing tumor angiogenesis and downregulating the HMGB1/RAGE/MEK/ERK signaling pathway^[2].
5-O-Methylvisammioside (3.5-7 mg/kg/day; i.p.; once daily; 14 days) dose-dependently alleviates DSS (HY-116282C)-induced ulcerative colitis in male Sprague-Dawley rats^[3].
5-O-Methylvisammioside (5-20 mg/kg; i.g.; single dose) reduces peak serum uric acid levels in single-dose HUA mice by up to 39.1% (10 mg/kg dose) and accelerates the return to baseline uric acid levels^[4].
5-O-Methylvisammioside (5-20 mg/kg; i.g.; once daily; 4 weeks) reduces serum uric acid and adenosine levels, improves liver/kidney function, alleviates intestinal inflammation and oxidative stress, restores intestinal barrier function, and normalizes intestinal CNT2 expression in chronic HUA mice^[4].