[The effect of rosuvastatin therapy on CCR2 expression in mononuclear cells and its upstream pathway]

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2016 Mar 8;32(3):202-206. doi: 10.13459/j.cnki.cjap.2016.03.003.
[Article in Chinese]

Abstract

Objective: To investigate the effect of rosuvastatin therapy on C-C chemokine receptor(CCR2)expression in mononuclear cells in patients with carotid atherosclerosis and explore the possible upstream mechanism.

Methods: Twenty patients without previous statin treatment were enrolled. Rosuvastatin were given 5 to 20 mg/day for 3 months. At baseline and 12 weeks, lipid profile and plasma monocyte chemotactic protein-1 (MCP-1) levels were examined. The mRNA and protein expressions of CCR2 in the mononuclear cells were measured with RT-PCR and flow cytometry, respectively. The mRNA and protein expression of peroxidase proliferator-activated receptor(PPAR β) were detected with RT-PCR and Western blot, respectively.

Results: After 3-months rosuvastatin treatment, the patients' low-density lipoprotein cholesterol (LDL-C) levels decreased significantly (P<0.01). Compared with baseline, the mRNA and protein expressions of CCR2 in the mononuclear cells showed significantly decrease, as well as plasma MCP-1 levels (P<0.05). Both mRNA and protein expressions of PPAR β in the mononuclear cells increased (P<0.05).

Conclusions: Rosuvastatin may attenuate MCP-1/CCR2 through PPARβ upstream pathway.

Keywords: CCR2; PPAR β; atherosclerosis; rosuvastatin.

MeSH terms

  • Atherosclerosis / drug therapy*
  • Chemokine CCL2 / metabolism*
  • Cholesterol, LDL / blood
  • Humans
  • Leukocytes, Mononuclear / drug effects*
  • PPAR-beta / metabolism
  • Receptors, CCR2 / metabolism*
  • Rosuvastatin Calcium / pharmacology*

Substances

  • CCL2 protein, human
  • CCR2 protein, human
  • Chemokine CCL2
  • Cholesterol, LDL
  • PPAR-beta
  • Receptors, CCR2
  • Rosuvastatin Calcium