Yi Zhong1, Tingrong Liu, Zhigang Guo. 1. Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Abstract
OBJECTIVE: This study was designed to identify the inhibitory effect of curcumin on ox-LDL-induced monocyte chemoattractant protein-1 (MCP-1) production and investigated whether the effects are mediated by mitogen-activated protein kinase (MAPK) and NF-κB pathways in rat vascular smooth muscle cells (VSMCs). METHODS: The VSMCs cells were pretreated with curcumin, before stimulation with ox-LDL. The ox-LDL-induced MCP-1 expression was determined by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). Intracellular signaling was investigated by Western blot. RESULTS: The concentrations of MCP-1 in cell supernatant and were upregulated by ox-LDL in a dose- and time-dependent manner. Additionally, curcumin decreased the expression of MCP-1 in a dose-dependent manner under treatment with ox-LDL (100 μg/ml). Signal transduction studies indicated that the ox-LDL-induced MCP-1 expression in VSMCs could be partly reversed by the inhibitor of p38 MAPK (SB203580) and NF-κB (BAY11-7082), whereas the ERK inhibitor (PD98059) and the JNK inhibitor (SP600125) had no effect. Western blot revealed that curcumin reduced ox-LDL- induced p38 MAPK phosphorylation and nuclear NF-κB p65 protein at the indicated concentration. CONCLUSION: Curcumin suppresses ox-LDL-induced MCP-1 expression in VSMCs via the p38 MAPK and NF-κB pathways, which suggests that the anti-inflammatory effect of curcumin is related to the down-regulation of MCP-1 expression and offers a new theoretical basis in the anti-inflammatory effects of curcumin.
OBJECTIVE: This study was designed to identify the inhibitory effect of curcumin on ox-LDL-induced monocyte chemoattractant protein-1 (MCP-1) production and investigated whether the effects are mediated by mitogen-activated protein kinase (MAPK) and NF-κB pathways in rat vascular smooth muscle cells (VSMCs). METHODS: The VSMCs cells were pretreated with curcumin, before stimulation with ox-LDL. The ox-LDL-induced MCP-1 expression was determined by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). Intracellular signaling was investigated by Western blot. RESULTS: The concentrations of MCP-1 in cell supernatant and were upregulated by ox-LDL in a dose- and time-dependent manner. Additionally, curcumin decreased the expression of MCP-1 in a dose-dependent manner under treatment with ox-LDL (100 μg/ml). Signal transduction studies indicated that the ox-LDL-induced MCP-1 expression in VSMCs could be partly reversed by the inhibitor of p38 MAPK (SB203580) and NF-κB (BAY11-7082), whereas the ERK inhibitor (PD98059) and the JNK inhibitor (SP600125) had no effect. Western blot revealed that curcumin reduced ox-LDL- induced p38 MAPK phosphorylation and nuclear NF-κB p65 protein at the indicated concentration. CONCLUSION:Curcumin suppresses ox-LDL-induced MCP-1 expression in VSMCs via the p38 MAPK and NF-κB pathways, which suggests that the anti-inflammatory effect of curcumin is related to the down-regulation of MCP-1 expression and offers a new theoretical basis in the anti-inflammatory effects of curcumin.
Authors: M Navab; S S Imes; S Y Hama; G P Hough; L A Ross; R W Bork; A J Valente; J A Berliner; D C Drinkwater; H Laks Journal: J Clin Invest Date: 1991-12 Impact factor: 14.808