Abstract:
:Curcumin, which is an extract from a traditional Chinese medicine, has previously been demonstrated to exhibit an anti‑atherosclerotic effect, which is closely associated with an increase in cholesterol efflux. However, it is unclear as to whether the increased effect is mediated by heme oxygenase (HO)‑1. Macrophages were treated with different concentrations of curcumin, HO‑1 inhibitor and small interfering (si)RNA in different experiments. Analysis of protein expression was conducted via western blotting. mRNA expression levels were measured using reverse transcription‑polymerase chain reaction. Antioxidant response element (ARE)‑driven promoter activity was measured by a dual‑luciferase reporter assay. The cholesterol efflux analysis was performed by fluorescence‑labelled cholesterol (NBD) using a multi‑label counter. In the present study, the results indicated that curcumin increased the cholesterol efflux from macrophages. Additionally, curcumin significantly upregulated HO‑1 expression. The HO‑1 inhibitor (zinc protoporphyrin) partly blocked this effect. Curcumin also promoted scavenger receptor class B type I (SR‑BI) and ATP‑binding cassette transporter A1 (ABCA1) expression. HO‑1 small interfering (si)RNA partly abolished the increased SR‑BI and ABCA1 expression induced by curcumin. Furthermore, the nuclear factor, erythroid 2 like 2 (Nrf2) expression in the nucleus was dose‑dependently increased by curcumin. Nrf2 siRNA successfully inhibited the curcumin‑induced HO‑1 expression. Curcumin significantly increased Nrf2‑driven luciferase activity. Overall, these data indicated that curcumin activates the Nrf2‑ARE signaling pathway and upregulates HO‑1 expression, which mediates SR‑BI and ABCA1 expression and thereby increases cholesterol efflux.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Zhong Y,Feng J,Fan Z,Li Jdoi
10.3892/mmr.2018.8577subject
Has Abstractpub_date
2018-04-01 00:00:00pages
6138-6143issue
4eissn
1791-2997issn
1791-3004journal_volume
17pub_type
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