Inhibitory effects of rosa roxburghii tratt juice on in vitro oxidative modification of low density lipoprotein and on the macrophage growth and cellular cholesteryl ester accumulation induced by oxidized low density lipoprotein
Cn. Zhang et al., Inhibitory effects of rosa roxburghii tratt juice on in vitro oxidative modification of low density lipoprotein and on the macrophage growth and cellular cholesteryl ester accumulation induced by oxidized low density lipoprotein, CLIN CHIM A, 313(1-2), 2001, pp. 37-43
Background: Rosa roxburghii tratt juice (RRTJ) administration has been show
n to significantly ameliorate atherosclerotic diseases in cholesterol-fed a
nimals. However, the mechanism for the antiatherogenic effect of RRTJ is no
t clear. Methods: We investigated the effects of RRTJ on in vitro oxidative
modification of LDL and on LDL-induced macrophage growth and cellular chol
esteryl ester (CE) accumulation. The effects of RRTJ on LDL oxidative modif
ication were assessed by relative electrophoretic migration, thiobarbituric
acid-reactive substance (TBARS) content, and the formation of conjugated d
ienes. The inhibition of RRTJ on oxidized LDL (Ox-LDL)-induced murine perit
oneal macrophage growth was evaluated by a cell-counting assay and an MTT a
ssay. The effect of RRTJ on Ox-LDL-induced cellular CE accumulation was exa
mined after macrophages were incubated with Ox-LDL in the presence of RRTJ.
To clarify the mechanism of the inhibitory effect of RRTJ on Ox-LDL-induce
d CE accumulation in macrophages, its capacity for cholesterol efflux from
macrophage-derived foam cells were examined. Results: We showed that RRTJ s
ignificantly reduced LDL oxidative susceptibility. In addition, RRTJ effect
ively suppressed Ox-LDL-induced macrophage growth and especially Ox-LDL-ind
uced CE accumulation in murine peritoneal macrophages by promoting cellular
cholesterol efflux. Conclusion: These results indicated that RRTJ exerted
its antiatherogenic effects largely due to its ability to inhibit the oxida
tive modification of LDL and to suppress the formation of foam cells. (C) 2
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