Ligustroflavone

Ligustroflavone is an orally active flavonoid compound. Ligustroflavone can be extracted from Ligustrum lucidum. Ligustroflavone antagonizes the calcium-sensing receptor (CaSR), inhibits the RIPK1/RIPK3/MLKL pathway, and downregulates TGF-β/Smad signaling. Ligustroflavone regulates calcium metabolism, protects bone tissue, reduces cerebral ischemic injury, and inhibits liver fibrosis. Ligustroflavone can be used in the study of diabetic osteoporosis, ischemic stroke, and liver fibrosis^[1][2][3]. IC50 & Target:CaSR^[1]. In Vitro:Ligustroflavone (0.1 nM-0.1 mM; 2-24 h) increases PTH release in primary rat parathyroid gland cells in a dose- and time-dependent manner^[1].
Ligustroflavone (25 μM) shows protective effects against hypoxia injury in PC12 cells, reducing LDH release^[2].
Ligustroflavone (25 μM; 24 h) reduces α-SMA and COL 1A1 expression in TGF-β₁-stimulated human hepatic stellate LX-2 cells^[3].
In Vivo:Ligustroflavone (5-20 mg/kg; i.p.; 3 times/week) inhibits diabetic osteoporosis in STZ (HY-13753)-induced diabetic male C57BL/6J mice by improving trabecular bone micro-architecture and reducing renal CaSR expression^[1].
Ligustroflavone (30 mg/kg; i.g.; 15 min before ischemia) reduces necroptosis in rat brain after ischemic stroke through inhibiting RIPK1/RIPK3/MLKL pathway^[2].
Ligustroflavone (5-20 mg/kg; i.p.; 3 times/week; 6 weeks) ameliorates CCl₄ (HY-Y0298)-induced liver fibrosis in mice by reducing collagen deposition and inhibiting TGF-β/Smad signaling^[3].