Effect of intensive rosuvastatin therapy on adhesion molecules and the upstream mechanism in patients with peripheral atherosclerosis.
- Author:
Ruixue DU
1
;
Ping YE
;
Guangtao YAN
;
Zihui DENG
;
Wentao LIANG
;
Honghong ZHANG
;
Miao GENG
;
Zikuan GUO
;
Hongmei WU
Author Information
- Publication Type:Journal Article
- MeSH: Atherosclerosis; drug therapy; metabolism; Cell Adhesion Molecules; metabolism; Female; Fluorobenzenes; administration & dosage; therapeutic use; Humans; Intercellular Adhesion Molecule-1; metabolism; Male; Middle Aged; Monocytes; drug effects; metabolism; PPAR gamma; metabolism; Pyrimidines; administration & dosage; therapeutic use; Rosuvastatin Calcium; Sulfonamides; administration & dosage; therapeutic use; Vascular Cell Adhesion Molecule-1; metabolism
- From: Journal of Southern Medical University 2012;32(11):1610-1614
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of intensive rosuvastatin therapy on adhesion molecules in patients with peripheral atherosclerosis and explore the possible upstream mechanism.
METHODSTwenty asymptomatic patients with peripheral atherosclerosis were enrolled and given 5-20 mg/day rosuvastatin for 3 months. Before and after the treatment, the lipid profile and plasma vascular cell adhesion molecule-1 (VCAM-1) levels were examined. The expression of intercellular adhesion molecule-1 (ICAM-1) in the mononuclear cells was measured using flow cytometry, and the mRNA and protein expressions of peroxisome proliferator-activated receptor γ (PPARγ) were detected using RT-PCR and Western blotting, respectively.
RESULTSCompared with the baseline levels, ICAM-1 expression decreased and PPARγ protein expression increased in the lymphocytes. Rosuvastatin therapy did not produce obvious effects on plasma VCAM-1 level or ICAM-1 expression in the monocytes in these patients.
CONCLUSIONRosuvastatin produces anti-inflammatory effects by decreasing the expression of ICAM-1 in mononuclear cells, and its upstream mechanism may involve the PPARγ pathway.