Protective effects of lusianthridin on hemin-induced low density lipoprotein oxidation and foam cell formation of raw 264.7 macrophage cells

Abstract

Oxidation of low-density lipoprotein (LDL) take parts in a crucial role in the pathogenesis of atherosclerosis. Hemin (iron (III)-protoporphyrin IX) is a degradation product of hemoglobin and cause oxidative stress-promoting vascular complications in thalassemia patients. Hemin was used as an oxidizing agent for LDL oxidation. Lusianthridin (LST) from Dendrobium venustum is a plant phenolic compound and possess antioxidant activity. The aim of this study is to evaluate the protective effect of lusianthridin on hemin-induced LDL oxidation (he-oxLDL) and foam cell formation in RAW 264.7 macrophage cell loaded with he-oxLDL treated with LST. Various concentrations of LST (0.25, 0.5, 1 and 2 µM) were preincubated with LDL for 30 min, then 5 µM hemin was added to initiate the oxidation and measured oxidative parameters at various times of incubation (0, 1, 3, 6, 12, 24 hr). Lipid peroxidation of LDL was measured by thiobarbituric reactive substance (TBARs) assay and relative electrophoretic mobility (REM). Lipid composition of LDL was analysed by using reverse phase HPLC. Foam cell formation with he-oxLDL in RAW 264.7 macrophage cells were detected by oil red O staining. The results demonstrated that LST at 1 and 2 µM were able to protect against lipid peroxidation in he-oxLDL by inhibition of TBARs formation, decreasing REM, preservation of cholesteryl arachidonate and cholesteryl linoleate level and decreased oxidized lipid products. In addition, exposure of he-oxLDL treated with 1 and 2 µM LST reduced the foam cell formation and decreased lipid content in macrophages significantly different from he-oxLDL untreated with LST (p<0.05 and p<0.0001, respectively). In conclusion, LST can protect LDL oxidation induced by hemin and showed the potential protective effect in foam cell formation in RAW 264.7 macrophage cell.