Journal
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
Volume 63, Issue 6, Pages 544-552Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0000000000000079
Keywords
curcumin; murine RAW264.7 macrophages; macrophages polarization
Funding
- National Natural Science Foundation of China [18110221]
- Nation Basic Research Program of China (973 Project) [2012CB517804]
- National Science Funds of Distinguished Young Scholars [81025002, 30871043]
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This study aimed to investigate the effects of curcumin on macrophages polarization and possible mechanism involved, and to analyze the molecular basis of its antiatherosclerosis activity. RAW264.7 macrophages (M0) and M1 macrophages were treated with curcumin at 0, 6.25, 12.5, and 25 mu mol/L with or without GW9662. Using real-time polymerase chain reaction and Western blot analysis, we examined the phenotype markers of M1 [iNOS, interleukin (IL)-1 beta, IL-6, and MCP-1] and M2 (KLF4, FIZZ1, and MGL1] macrophages. Curcumin reduced the expression of the M1 phenotype markers and upregulated the expression of proliferator-activated receptor gamma in M0 and M1 macrophages and IKB alpha in M1 macrophages. When M1 macrophages were incubated with curcumin and GW9662, the expression of the M1 phenotype markers was decreased, while IKB alpha was upregulated. The expression of the M2 phenotype markers in M0 and M1 macrophages was upregulated after the curcumin treatment. When M0 and M1 macrophages were incubated with curcumin and GW9662, the expression of the M2 phenotype markers was reduced. Curcumin inhibited the M1 inflammation phenotype as a result of the direct activation of IKB alpha and polarized the macrophages to become M2 phenotype through the activation of proliferator-activated receptor gamma. These findings provide new clues to develop new drug therapy for atherosclerosis.
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