Atorvastatin Attenuates CCL20 Expression via the NF-κB Pathway in OxLDL-Induced Macrophages: A Potential Mechanism of Antiatherosclerosis

Abstract

Background: Emerging evidence indicates that the chemokine C-C motif ligand 20 (CCL20) promotes atherosclerosis via a chemo-attraction process. Statins improve atherosclerosis by inhibiting chemokine expression. Although the regulatory mechanisms of CCL20 have been investigated in other cells, they have not been clarified in macrophages. Moreover, the statin-induced regulation of CCL20 has not been studied previously. Therefore, this study explored the regulatory mechanism of CCL20 in oxidized low-density lipoprotein (oxLDL)-induced macrophages and the effect of statins on CCL20. Methods: CCL20 expression was tested after applying atorvastatin to interfere with oxLDL-induced macrophages, inhibiting nuclear factor-kappa B (NF-κB) activity in oxLDL-induced macrophages and the atorvastatin intervention model, and after transfecting a CCL20 overexpression plasmid into RAW 264.7 cells, after which NF-κB activity was also tested. Results: The results showed that atorvastatin downregulates CCL20 in oxLDL-induced macrophages, the NF-κB pathway participates in CCL20 regulation, and CCL20 overexpression in macrophages activates NF-κB. Conclusions: The results suggest that the NF-κB pathway is involved in regulating CCL20 expression in macrophages. Moreover, atorvastatin may regulate CCL20 to exert anti-inflammatory functions, indicating that the NF-κB/CCL20 signaling pathway represents a potential antiatherosclerosis target.