Abstract
ObjectiveAccumulation of foam cells in intima is the hallmark of early stage atherosclerotic lesion. Ginkgo Biloba extract (EGb761) has been reported to exert excellent anti‐oxidative and anti‐inflammatory properties in the development of atherosclerosis, yet the effect and the molecular mechanisms of EGb on the formation of macrophage foam cells are not fully understood.Methods and resultsTreatment with EGb761 resulted in a dose‐dependent decrease in oxLDL‐mediated cholesterol accumulation in macrophages, a result that was due to a decrease in cholesterol uptake and an increase in cholesterol efflux. Additionally, EGb treatment significantly decreased the mRNA and protein expression of class A scavenger receptor (SR‐A), while EGb had no effect on the expression of CD36, SR‐BI or ATP‐binding cassette (ABC) transporter G1. Furthermore, EGb increased the protein stability of ABCA1 by reducing calpain activity without affecting ABCA1 mRNA expression. Moreover, small interfering RNA (siRNA) targeting heme oxygenase‐1 (HO‐1) abolished the EGb‐induced protective effects on the expression of SR‐A and ABCA1 and calpain activity. Consistently, EGb‐mediated suppression on lipid accumulation in foam cells was also abrogated by HO‐1 siRNA.ConclusionEGb confers the protection from the formation of foam cells by an HO‐1‐dependent regulation on cholesterol homeostasis in macrophages.
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