Rhamnocitrin

Rhamnocitrin is an anti-inflammatory and antioxidant agent that targets STIM-1, NFATc3 and MAPK pathways and can scavenge DPPH (IC₅₀=28.38 mM). Rhamnocitrin selectively inhibits oxidative stress and inflammatory responses in vascular endothelial cells and neurons. Rhamnocitrin up-regulates miR-185 to inhibit STIM-1-mediated store-operated calcium entry (SOCE), thereby blocking NFATc3 nuclear translocation and downstream inflammatory factor expression, while inducing heme oxygenase HO-1 expression and regulating the ERK/p38 MAPK pathway, inhibiting antioxidant and pro-inflammatory cytokines (such as IL-6, IL-8) and adhesion molecules (such as ICAM-1, VCAM-1). Rhamnocitrin can be used in the study of endothelial-related inflammatory diseases (such as sepsis, acute lung injury, atherosclerosis) and neuroprotection (such as oxidative damage of PC12 cells)^[1][2][3][4]. In Vitro:Rhamnocitrin (40-80 μM; 48 h) significantly reduces apoptosis in serum deprivation-induced rat adrenal pheochromocytoma PC12 cells, and has no significant effect on STIM-1/Orai-1-mediated SOCE and downstream NFATc3 signaling^[2].
Rhamnocitrin (0.1-10 μM; 24 h) inhibits the expression of IL-6, IL-8, MCP-1, ICAM-1, VCAM-1 and PAI-1 in a concentration-dependent manner in LPS-induced human umbilical vein endothelial cells (HUVECs) experiments, and inhibits STIM-1-mediated store-operated calcium entry (SOCE)^[3].
In Vivo:After oral administration of 10 mL/kg A. complanatus extract (equivalent to 17.6 mg/kg Rhamnocitrin) to rats, collects blood (approximately 0.3 mL) at 0, 0.083, 0.167, 0.25, 0.333, 0.5, 0.75, 1, 2, 4, 6, 9, and 12 hours after administration from the ocular vein for analysis, under ether anesthesia. The results shows that the plasma concentration of Rhamnocitrin reached its maximum at 0.65 hours, with an average C_max of 29.57 ng/mL^[1].