C1q/ tumor necrosis factor-related protein 9 decreases pro-inflammatory cytokines expression in macrophage cells by inhibiting nuclear factor-κB translocation

Abstract

Objective To investigate the anti-inflammatory effect of C1q/ tumor necrosis factor (TNF)-related protein 9 (CTRP9) in RAW264.7 mouse macrophage cells treated with oxidized low density lipoprotein (oxLDL), and to explore its mechanism. Methods RAW264.7 mouse macrophage cells were divided into three groups: the control group, the oxLDL group (treated with oxLDL) and the gCTRP9+ oxLDL group (pretreated with recombinant globular domain of CTRP9 and stimulated by oxLDL). Foam cells were detected by oil red O staining. Western blot was used to detect the expressions of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1). In addition, the expression levels of NF-κB p65 in cytoplasm and nucleus proteins extraction were both determined. Results The relative levels of MCP-1 and NF-κB were increased in the oxLDL group as compared with the control group (1.66±0.09 vs. 1.03±0.10, 0.52±0.11 vs. 1.03±0.06, both P<0.05). The expression levels of TNF-α and MCP-1 were decreased in gCTRP9+ oxLDL group as compared with the oxLDL group (both P<0.05). The expression level of NF-κB p65 in nucleus 2 and 8 h after treatment was lower in the gCTRP9+ oxLDL group than in the oxLDL group (1.03±0.06 vs. 0.17±0.10, 0.31±0.03, both P<0.05). Conclusions oxLDL may induce the expressions of inflammatory cytokines of TNF-α and MCP-1 in macrophage cells. gCTRP9 pretreatment could reduce the oxLDL-induced pro-inflammatory effect and nuclear factor-κB translocation may be involved in this process, which suggests that gCTRP9 may play a protective role in anti-inflammatory and anti-atherosclerosis. Key words: Tumor necrosis factor; Atherosclerosis